Painful Foot and Ankle

American Association of Electrodiagnostic Medicine

Tracy A. Park, MD David R. Del Toro, MD Mohammad A. Saeed, MD, MS Atul T. Patel, MD, MHSA Mark E. Easley, MD

2004 AAEM COURSE C AAEM 51st Annual Scientific Meeting Savannah, Georgia Painful Foot and Ankle

Tracy A. Park, MD David R. Del Toro, MD Mohammad A. Saeed, MD, MS Atul T. Patel, MD, MHSA Mark E. Easley, MD

2004 COURSE C AAEM 51st Annual Scientific Meeting Savannah, Georgia

PRINTED BY JOHNSON PRINTING COMPANY, INC. ii Painful Foot and Ankle

Faculty

Tracy A. Park, MD Mohammad A. Saeed, MD, MS Physiatrist Clinical Associate Professor Medical Rehabilitation Associates Department of Rehabilitation Medicine Milwaukee, Wisconsin University of Washington Dr. Park is currently in private practice at Medical Rehabilitation Seattle, Washington Associates in Milwaukee. In addition, he is an attending physiatrist at both Dr. Saeed received his specialty training in physical medicine and rehabil- St. Joseph’s Regional Medical Center and St. Michael’s Hospital in itation at the University of Washington in Seattle, Washington. Following Milwaukee as well as an attending physiatrist at Elmbrook Memorial residency, he served in the United States Army at Madigan Army Medical Hospital in Brookfield, Wisconsin. He performed a physical medicine and Center in Tacoma, Washington, and from 1981-1982 as Chief of the rehabilitation residency at the Rehabilitation Institute of Chicago and went Physical Medicine Service. For the past 20 years, he has been in private on to perform a fellowship in electrodiagnostic medicine at the Medical practice, now as senior partner with Electrodiagnosis and Rehabilitation College of Wisconsin. Dr. Park is board-certified by the Amercan Board of Associates of Tacoma. He has published several articles and abstracts on a Electrodiagnostic Medicine (ABEM), the American Board of Physical broad range of electrodiagnostic topics. Current clinical interests include Medicine and Rehabilitation, and the National Board of Medical lower extremity entrapment neuropathies, particularly focal neuropathies Examiners. He is an active member of the Association of Academic of the foot and tarsal tunnel syndrome. Dr. Saeed has often been invited Physiatrists and the AAEM. He has served on AAEM’s Education faculty at the AAEM annual meetings and has actively been involved on Committee and has been an oral examiner for the American Board of the Education, Workshop, Training Program, and Program Committees. Electrodiagnostic Medicine. He is also a manuscript reviewer for the He is a long time fellow of both the AAEM and AAPM&R, and has been Archives of Physical Medicine and Rehabilitation. an examiner for the American Board of Electrodiagnostic Medicine for many years. David R. Del Toro, MD Associate Professor Atul T. Patel, MD, MHSA Department of Physical Medicine and Rehabilitation Physiatrist Medical College of Wisconsin Kansas City Bone and Joint Clinic Milwaukee, Wisconsin Kansas City, Missouri Dr. Del Toro earned his medical degree at Indiana University School of Dr. Patel earned a bachelor of science in chemical engineering at the Medicine and performed an internship in general surgery at Methodist University of Houston before entering medical school at Baylor College of Hospital of Indiana in Indianapolis. He then performed a residency in Medicine. He then studied rehabilitation medicine at the University of physical medicine and rehabilitation at the Medical College of Wisconsin, Washington and later became Residency Program Director for the and is now an associate professor there. He is a member of several societies, Department of Rehabilitation Medicine at the University of Kansas including the American Academy of Physical Medicine and Rehabilitation Medical Center. He is currently a physiatrist at the Kansas City Bone and (AAPMR) and the AAEM. Dr. Del Toro has served on the AAEM’s Tarsal Joint Clinic in Kansas City. Dr. Patel is board-certified by the American Tunnel Syndrome Task Force, Young Physicians Task Force, and the Board of Physical Medicine and Rehabilitation (ABPMR), ABPMR sub- AAEM Workshop Committee. He is also an oral examiner for the speciality of spinal cord injury medicine, the American Board of American Board of Electrodiagnostic Medicine. Dr. Del Toro has also been Independent Medical Examiners, and the ABEM. He is a member of an abstract reviewer for AAPMR and is currently a manuscript reviewer for several professional organizations, including the American Academy of the Archives of Physical Medicine and Rehabilitation. Physical Medicine and Rehabiliation, the Association of Academic Physiatrists, the American Geriatric Society, and the American Academy of Disability Evaluating Physicians. He is also active in the AAEM, and has been the chair of the Tarsal Tunnel Task Force and a member of the Workshop, Program, and the Quality Assurance committees. Dr. Patel recently earned his Master of Health Services Administration degree.

Course Chair: Tracy A. Park, MD

The ideas and opinions expressed in this publication are solely those of the specific authors and do not necessarily represent those of the AAEM. AAEM Course Painful Foot and Ankle iii

Mark E. Easley, MD Assistant Professor Division of Orthopaedic Surgery Duke University Medical Center Durham, North Carolina Dr. Easley is currently an assistant professor in the Division of Orthopaedic Surgery at Duke University Medical Center. He is also a consultant to several area medical centers. Dr. Easley attended medical school at the University of Virginia and went on to perform a foot/ankle fellowship at Union Memorial Hospital in Baltimore and a knee fellowship at Insall- Scott-Kelly Institute in New York. He is a member of the American Academy of Orthopaedic Surgeons, the Eastern Orthopaedic Association, and the American Orthopaedic Foot and Ankle Society, among others. In 2003, Dr. Easley was chosen as the American Orthopaedic Association’s ABC Traveling Fellow.

Authors had nothing to disclose.

Please be aware that some of the medical devices or pharmaceuticals discussed in this handout may not be cleared by the FDA or cleared by the FDA for the specific use described by the authors and are “off-label” (i.e., a use not described on the product’s label). “Off-label” devices or pharmaceuticals may be used if, in the judgement of the treating physician, such use is medically indicated to treat a patient’s condition. Information regarding the FDA clearance status of a particular device or pharmaceutical may be obtained by reading the product’s package labeling, by contacting a sales representative or legal counsel of the manufacturer of the device or pharmaceutical, or by contacting the FDA at 1-800-638-2041. iv AAEM Course v Painful Foot and Ankle

Contents

Faculty ii Objectives v Course Committee vi

Peroneal Nerve Entrapments: Deep and Superficial 1 Tracy A. Park, MD

Baxter’s Nerve Entrapment 9 David R. Del Toro, MD

Tarsal Tunnel Syndrome 17 Mohammad A. Saeed, MD, MS

Nonneurogenic Causes of Foot Pain 27 Atul T. Patel, MD, MHSA

Surgical Management of Entrapment Neuropathies in the Foot, Including Indications and Outcomes 33 Mark E. Easley, MD CME Self-Assessment Test 53 Evaluation 55 Future Meeting Recommendations 57

O BJECTIVES—After attending this course, the participant will be able to (1) discuss the anatomy of the foot as it relates to entrapment of, and electrodiagnostic study of, the terminal branches of the tibial nerve, deep peroneal nerve, and superficial peroneal nerve, (2) discuss the anatomy of the foot as it relates to common non-neurogenic causes of foot pain, (3) discuss the clinical presentation and differential diagnosis of tarsal tunnel syndrome, Baxter’s nerve entrapment, “anterior” tarsal tunnel syndrome, and superficial peroneal nerve entrapment, (4) devise and perform an electrodiagnostic examination that effectively addresses suspected isolated nerve entrapments in the foot, and (5) discuss the surgical and nonsurgical approaches to the management of neurogenic and nonneurogenic foot pain. P REREQUISITE—This course is designed as an educational opportunity for residents, fellows, and practicing clinical EDX consultants at an early point in their career, or for more senior EDX practitioners who are seeking a pragmatic review of basic clinical and EDX prin- ciples. It is open only to persons with an MD, DO, DVM, DDS, or foreign equivalent degree. A CCREDITATION S TATEMENT—The AAEM is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education (CME) for physicians. CME CREDIT—The AAEM designates attendance at this course for a maximum of 3.5 hours in category 1 credit towards the AMA Physician’s Recognition Award. This educational event is approved as an Accredited Group Learning Activity under Section 1 of the Framework of Continuing Professional Development (CPD) options for the Maintenance of Certification Program of the Royal College of Physicians and Surgeons of Canada. Each physician should claim only those hours of credit he/she actually spent in the activity. The American Medical Association has determined that non-US licensed physicians who participate in this CME activity are eligible for AMA PMR category 1 credit. vi

2003-2004 AAEM COURSE COMMITTEE

Kathleen D. Kennelly, MD, PhD Jacksonville, Florida

Thomas Hyatt Brannagan, III, MD Dale J. Lange, MD T. Darrell Thomas, MD New York, New York New York, New York Knoxville, Tennessee

Kimberly S. Kenton, MD Andrew Mazur, MD Bryan Tsao, MD Maywood, Illinois Portsmouth, Rhode Island Shaker Heights, Ohio

Christopher J. Standaert, MD Seattle, Washington

2003-2004 AAEM PRESIDENT

Lois Margaret Nora, MD, JD Rootstown, Ohio Peroneal Nerve Entrapments: Deep and Superficial

Tracy A. Park MD Medical Rehabilitation Associates Milwaukee, Wisconsin

INTRODUCTION Both DPN branches pass deep to the inferior extensor retinaculum. The medial branch courses distally in the foot, passing an Much attention in the electrodiagnostic world has been dedi- average of 2.9 mm lateral to the first tarsometatarsal joint,31 and cated to compromise of the common peroneal nerve (CPN) at crossing beneath the extensor hallucis brevis tendon in the fore- the fibular head. However, the individual branches of the foot. Before terminating as the cutaneous innervation to the CPN—the deep peroneal nerve (DPN) and superficial peroneal dorsal first web space, the otherwise sensory medial branch may nerve (SPN)—can be selectively involved more distally in the send some motor twigs to the first dorsal interosseus pedis30 in as leg. Because these entrapments present with a more vague and many as 92% of feet.3 The lateral branch innervates the EDB less dramatic clinical picture than those of the CPN, they have and sends articular twigs to multiple joints in the midfoot and only infrequently been the subject of studies in the electrodiag- forefoot. nostic literature. The purpose of this manuscript is to address compression at the ankle of the DPN (anterior tarsal tunnel syn- Mechanism of Compression: Inferior Extensor Retinaculum drome) and the SPN, including anatomical considerations, clinical presentation, electrodiagnosis, and treatment. One or both of the DPN branches can be compromised where they pass beneath the inferior extensor retinaculum in the anterior ankle. Although this condition has been named the “ante- ANTERIOR TARSAL TUNNEL SYNDROME rior tarsal tunnel syndrome,” (ATTS) this is a bit of a misnomer, since there is no actual anatomic “anterior tarsal tunnel,” but Deep Peroneal Nerve Anatomy rather a convex bony surface blanketed by the broad inferior extensor retinaculum.17 After branching from the CPN just distal to the fibular head, the DPN passes through the anterior compartment between the in- Although classic ATTS is due to compression of the DPN as it dividual muscles of the anterior tibial region. In the leg, the passes deep to the inferior extensor retinaculum, a nearly identi- DPN is a major contributor of articular branches to the ankle cal clinical picture can result from compromise of the DPN due joint.42 Studies by Horwitz,23 and Lawrence and Botte31 revealed to a number of other causes. These include ischemia from de- that the DPN divides into medial and lateral branches 1.3 cm compression illness,41 talar exostoses,16 dorsal foot contusions,34 proximal to the mortise (Figure 1). A medial (sensory) branch ganglia on tendons in the tunnel, pes cavus, tight shoe laces, then passes directly over the talonavicular joint capsule, while a ski boots,27 combat boots, repetitive ankle plantarflexion lateral (motor) branch swings laterally to the extensor digitorum in ballet dancers, schwannoma,43 the performing of brevis (EDB).31 Namaz,4 trauma or post-traumatic changes (such as fractures or 2 Peroneal Nerve Entrapments: Deep and Superficial AAEM Course

Examination may reveal sensory deficits over the dorsal first web space if the medial branch is involved.5,7,15,22,29,34 Examination of the lateral branch is more of a problem. Even severe isolated weakness of the EDB is nearly impossible to detect clinically, but it is often accompanied by visible atrophy of this muscle when compared to the unaffected foot, thereby giving a clue to lateral branch involvement.1,5,7,15,22,29,30,34 The DPN at the inferior extensor retinaculum may display a Tinel sign or tenderness to palpation.7,15,29,34 Placing the patient’s foot in a “high-heeled shoe” position with the toes dorsiflexed and the ankle plantarflexed may provoke or reproduce the symptoms.7,34

Electrodiagnostic Studies

Although motor nerve conduction studies (NCSs) of the DPN to the EDB have been described,13,32 anatomic details—particularly regarding the placement of E1—are universally vague. Mostly, these reports call for positioning the E1 electrode “over the EDB muscle”13 with no anatomic landmarks given. This Figure 1 Terminal course of the deep peroneal nerve (DPN). technique falls apart in the face of an atrophic muscle—one for Proximal to the inferior extensor retinaculum, the DPN typically which the E1 placement is, unfortunately, the most critical. To divides into a medial branch, innervating the first dorsal web remedy this problem, this author and colleagues conducted an space, and a lateral branch, innervating the extensor digitorum electrophysiologic mapping study of the EDB on 10 normal brevis. (From Park TA, Del Toro DR: Electrodiagnostic evaluation of feet, and matched these findings to the anatomy of the foot sur- the foot. Phys Med Clin of N Am 9(4):891, 1998. Adapted from rounding this muscle. It was found that there were no false Liveson JA: Peripheral Neurology: Case Studies in Electrodiagnosis, motor points in the EDB of any of these feet, and that the 2nd edition. Philadelphia, FA Davis, 1991, p 53; with permission.) optimal E1 site (based on compound muscle action potential [CMAP] amplitude) did not coincide with the most prominent point of the EDB belly, determined on each foot prior to the inversion-plantarflexion ankle sprains), and traction placed on mapping study. This optimal E1 site corresponded anatomically the DPN under the inferior extensor retinaculum by the “high- to a point 1 cm distal and 1 cm lateral to the intersection of the heeled shoe” position (toes dorsiflexed and ankle plan- extensor digitorum longus tendon to the little toe and the calca- tarflexed).1,7,9,11,15,30 In addition, isolated entrapment of the neocuboid ridge (Figures 2 and 3). With stimulation of the medial branch can occur at the first tarsometatarsal joint, either DPN at the ankle, this grid site had a mean distal latency with as a result of a bone spur or bony ridge at this site36,38 or through the smallest standard deviation (4.3 ± 0.7 ms at 8 cm), and also compression by the overlying extensor hallucis brevis the largest mean CMAP amplitude (7.7 ± 1.6 mV). tendon.14,25,40 The importance of locating the ideal E1 site becomes apparent Clinical Presentation when considering the high amplitude zone (HAZ) for the EDB. The HAZ is the region over a muscle in which the amplitude of Anterior tarsal tunnel syndrome presents with vague, often dis- the recorded CMAP is at least 80% of the amplitude of that abling complaints caused by a lesion of the DPN, or one of its muscle’s largest CMAP. This ideal recording area for the EDB is branches, at the ankle. Patients’ complaints are mostly sensory in much smaller than those of the typical intrinsic muscles used for nature, since they rarely notice weakness of the EDB. Aching or median, ulnar, or tibial nerve motor NCSs.48 Therefore, the ex- tightness over the anterior ankle and dorsal foot suggests in- amining physician must use particular care when positioning the volvement of the lateral branch of the DPN, whereas numbness E1 electrode over the EDB, or the amplitude may be erro- and paraesthesias in the first dorsal web space indicate medial neously small. branch compromise.5,22,29,30,34 The symptoms may be worse when the patient is at rest7,29 or during weightbearing. In reports of ATTS, abnormalities for DPN motor NCSs Worsening of the pain may cause it to extend proximally into the include an abnormally small or delayed CMAP,1,5,7,22,29,30,34 as lower leg.30 The patient may be awakened by the symptoms at well as focal conduction block with serial “short-segment” stim- night,1,5,7,15,22,29,30,34 relieving them by shaking or moving the af- ulation across the anterior ankle.5 fected foot.29 AAEM Course Painful Foot and Ankle 3

Figure 2 Optimal E1 site for recording the deep peroneal nerve response over the extensor digitorum brevis. The tendons of the extensor digitorum longus are most easily palpated by having the patient dorsiflex the toes and ankle. The calcaneocuboid ridge is best palpated with the ankle in passive plantarflexion/inversion and the toes relaxed. Electrode placement is approximately 1 cm lateral and 1 cm distal to the junction between the calcaneocuboid ridge and the long extensor tendon to the little toe. (Adapted from Liveson JA, Ma DM: Laboratory Reference for Clinical Neurophysiology. Philadelphia, FA Davis, 1992, p 203; with permission.)

A sensory nerve conduction technique has been described for the Figure 3 Bones of the right foot, showing the relationship DPN, recording antidromically over the first dorsal web space between the origin of the extensor digitorum brevis (EDB) and the while stimulating above the ankle.13,32 Extensive signal averaging calcaneocuboid ridge. The EDB extends over this ridge on its way to is generally required, the resulting sensory nerve action potential the toes, and the bulk of the muscle is located just distal to the (SNAP) is extremely small, and is, in fact, often too small to ridge. (Adapted from Chu-Andrews J, Johnson R: Electrodiagnosis: record in normal individuals. If this technique is used, it is there- An Anatomical and Clinical Approach. Philadelphia, JB Lippincott, fore imperative to perform it on the asymptomatic foot for com- 1986; with permission.) parison. A significant side-to-side difference in the latency or amplitude suggests compression of the DPN at the ankle.

In an isolated DPN lesion at the ankle, motor and sensory NCSs this muscle. A better approach is to insert the needle near the of the other nerves to the foot, including the SPN, should be lateral edge of the muscle, angling the needle medially over the normal. dorsum of the foot. The insertion site should be just anterior to the calcaneocuboid ridge, where the main bulk of the muscle is The needle EMG examination technique for the EDB is often located, and just medial to the peroneus brevis tendon, which is inadequately described. Some reference books for needle EMG easily palpated near the lateral edge of the foot when the foot is leave this muscle out entirely.21 Those that do include the EDB actively everted (Figures 3 and 4). This technique allows the recommend approaching the muscle perpendicularly, at the needle to pass deep to the long extensor tendons and explore all most prominent point of the muscle belly.8,12 This angle seems four bellies of the EDB, rather than just the belly to the fourth to unacceptably underutilize the flat, fan-shaped geometry of toe. 4 Peroneal Nerve Entrapments: Deep and Superficial AAEM Course

Needle EMG findings reported in ATTS have included evidence Although published studies have reported prolonged insertional of denervation in the EDB in the form of prolonged insertional activity in the EDB in a considerable proportion of normal activity, abnormal spontaneous activity,5,7,22,29,34 increased motor feet,18,20,49 this author has not found this to be the case in his unit action potential (MUAP) complexity and duration,5,29 and practice. Prolonged insertional activity is seldom seen in normal decreased motor unit recruitment.5,22,29,34 No such abnormalities feet, and frank spontaneous activity quite rarely—certainly not should be seen in tibial-innervated intrinsic foot muscles, in the enough to justify deferring needle EMG of the foot on these EDB of the unaffected foot, or in leg muscles innervated by the grounds. DPN. Treatment

Conservative management may include changing the patient’s foot-wear to flat-heeled, more loose-fitting shoes,7,29,30 as well as administering a local steroid injection.7,29,30,34 If these measures fail, surgical treatment—consisting of exploration and decompression of the DPN under the inferior extensor retinaculum— can result in improvement of symptoms.5,7,29,30,34

SUPERFICIAL PERONEAL NERVE ENTRAPMENT

Superficial Peroneal Nerve Anatomy

After leaving the CPN, the SPN courses deep to the peroneal muscles in the lateral compartment in the upper third of the leg, although it can occasionally cross instead to the anterior compartment.2 The SPN then pierces the deep crural fascia approximately 13 cm proximal to the tip of the lateral malleolus and divides about 2 cm later into the medial and intermediate dorsal cutaneous branches2 (Figure 5). Both of these branches cross the anterior ankle superficial to the inferior extensor retinaculum on their way to the dorsum of the foot. The medial dorsal cutaneous branch divides into three branches that terminate in the dorsum of the first, second, and third toes, while the intermediate dorsal cutaneous branch innervates the dorsum of the adjacent sides of the third and fourth toes.42 Both branches also provide innervation to most of the dorsum of the foot.

Mechanism of Entrapment: Anterior Fascia of Leg

The SPN is vulnerable to entrapment as it exits the deep crural fascia about 13 cm proximal to the lateral malleolus.2 Reported Figure 4 Needle approach to the extensor digitorum brevis etiologies include a sharp fascial edge,33 varicose veins,46 com- (EDB). The needle is inserted just medial to the peroneus brevis pression at the exit site due to anterolateral compartment syn- tendon, which is prominently displayed when the ankle is actively 19,46,47 26,46 19,35,46 everted. The angle of the path of the needle is very shallow, taking drome, ankle sprain, muscle herniation, a 6,46 it across the dorsum of the foot and beneath the long extensor lipoma/fat nodule at the break in the deep fascia, injury to the 46,47 tendons, thus allowing it to explore the four bellies of the EDB. SPN during anterior compartment fasciotomy, and pro- (Adapted from Liveson JA: Peripheral Neurology: Case Studies in longed kneeling and squatting over many years.39 Many of the Electrodiagnosis, 2nd edition. Philadelphia, FA Davis, 1991, p 53; reported cases have been in athletes.10,19,35,45 with permission.) AAEM Course Painful Foot and Ankle 5

colleagues24 described an antidromic technique for studying the individual medial and intermediate dorsal cutaneous branches separately. More recently, Oh and colleagues37 devised an NCS method that examines the digital twigs of the medial and intermediate dorsal cutaneous branches with electrodes over the digital twigs to the second and third toes (medial dorsal cutaneous) and the fourth and fifth toes (intermediate dorsal cutaneous branch). This NCS technique can be performed either orthodromically or antidromically.

Nerve conduction study testing should include one or both SPN branches on the affected side, as well as the unaffected side if needed for comparison. Stimulation electrodes and recording electrodes should be applied on opposite sides of the SPN exit point from the deep fascia.

Needle EMG examination should include at least the superficial peroneal innervated muscles (i.e., peroneus longus and peroneus brevis) of the affected leg, as well as broader testing to exclude a possible lumbosacral radiculopathy. Figure 5 Distal course of the superficial peroneal nerve (SPN) and its terminal branches. Before branching into the medial and intermediate dorsal cutaneous nerves, the SPN exits the deep crural Diagnostic electrophysiologic findings for superficial peroneal fascia in the lower leg, a site of entrapment of this nerve. (Adapted neuropathy may include a prolonged distal latency (or decreased 45,46,47 from Liveson JA, Ma DM: Laboratory Reference for Clinical distal NCV) in the affected SPN branch, although a Neurophysiology. Philadelphia, FA Davis, 1992, p 203; with per- reduced SNAP amplitude may be more common.15,44 All needle mission.) EMG findings are typically normal.15,46

Treatment

Clinical Presentaion Surgical intervention usually consists of releasing the fascial band at the deep fascial exit,6,26,33,35,39 reducing any muscle hernia- Superficial peroneal nerve entrapment usually presents with tion,19 or removing any fat nodule.6 A fasciotomy may also be smoldering pain over the lateral ankle and dorsum of the foot. performed if there is an associated anterolateral compartment Interestingly, only about one-third of patients complain of syndrome.19 In a report by Styf, 75% of patients remain im- numbness or paresthesias over the dorsum of the foot.19,33 Often, proved 36 months after surgery; the number is lower in ath- there is only vague pain laterally at about the junction between letes.46 the middle and distal thirds of the leg.6,26 Pain may radiate as far proximally as the thigh.28,33 Symptoms usually worsen with weightbearing6,33,35 and improve with rest,6,19,35 and do not tend CASE REPORT to worsen at night. Some patients actually report a localized mass in the distal anterolateral leg.19,35 History

Physical examination will show local tenderness19,26,33,46 and a A 35-year-old white female presented with a 5-year history of Tinel’s sign over the fascial exit site.6,19,26,33,45,46 A palpable fascial stable chronic low back pain that increased significantly in the defect or bulge is often detectable.6,19,26,35 Pain may be provoked month prior to her visit. There was no clear exacerbating event. by resisted active ankle dorsiflexion/eversion or by passive ankle The pain was constant and extended from her low back across plantarflexion/inversion.45,46 There is frequently diminished sen- her right buttock and right hip, over her anterior right thigh, and sation over the dorsum of the foot.19,26,46 down her medial right shin. An epidural steroid injection reduced the pain significantly, except for the medial shin pain, Electrodiagnostic Studies which continued as a constant aching accompanied by tingling. Because of her symptoms, she was on medical leave from her A number of investigators have described orthodromic and an- sedentary job since the symptoms began, and she has a sedentary tidromic NCS techniques for the SPN.32 In addition, Izzo and lifestyle. 6 Peroneal Nerve Entrapments: Deep and Superficial AAEM Course

Physical Examination SUMMARY

The patient was a morbidly obese white female who moved gin- The main difficulty in diagnosing isolated distal entrapment of gerly, and had puffy feet, though no frank pitting edema. Muscle either the DPN or the SPN is probably their typically nonspe- stretch reflexes were 2+ throughout her lower extremities. There cific symptoms. These disorders should be kept in mind when- was no definite weakness in her lower extremities. Perception of ever a patient complains of vague aching or discomfort in the pinprick was decreased in the right lateral thigh and knee, and lower leg or ankle. With an accurate knowledge of the anatomy also in the right dorsal first web space. of these nerves, one can then bring the diagnosis into clearer focus with a clinical assessment that takes their entrapments into Nerve Conduction Studies consideration. Appropriate electrodiagnostic testing, correctly performed, can then confirm or rule out these diagnostic possi- The right deep peroneal motor NCS had a distal latency of 8.4 bilities. ms, an amplitude of 0.7 mV, and a conduction velocity of 41 m/s across the leg. Short segment inching technique performed across the ankle demonstrated no focal delay in conduction or REFERENCES loss of amplitude. The left deep peroneal motor NCS had a distal latency of 4.7 ms and an amplitude of 9.0 mV. The re- 1. Adelman KA, Wilson G, Wolf JA. Anterior tarsal tunnel syndrome. maining NCSs were normal, including the right tibial motor, J Foot Surg 1998;27:299-302. 2. Adkison DP, Bosse MJ, Gaccione DR, Gabriel KR. Anatomical vari- right sural sensory, and bilateral tibial H reflexes. ations in the course of the superficial peroneal nerve. J Bone Joint Surg Am 1991;73:112. Needle Electromyography 3. Akita K, Sakamoto H, Sato T. Lateromedial and dorsoplantar borders among supplying areas of the nerves innervating the intrinsic muscles Muscles of the right lower extremity and right lumbosacral of the foot. Anat Rec 1999;225:465-470. paraspinal muscles were explored. The EDB had prolonged in- 4. Akyuz G, Us O, Turan B, Kayhan O, Canbulat N, Yilmar IT. Anterior tarsal tunnel syndrome. Electromyogr Clin Neurophysiol sertional activity, 3+ spontaneous activity, and reduced motor 2000;40:123-128. unit recruitment increased firing frequencies. Motor unit action 5. Andresen BL, Wertsch JJ, Stewart WA. Anterior tarsal tunnel syn- potentials had increased complexity and duration, as well as in- drome. Arch Phys Med Rehabil 1992;73:1112-1117. creased amplitudes of up to 6 mV. 6. Banerjee T, Koons DD. Superficial peroneal nerve entrapment: Report of two cases. J Neurosurg 1981;55:991-992. 7. Borges LF, Hallett M, Selkoe DJ, Welch K. The anterior tarsal tunnel Abnormalities were also seen in the vastus lateralis (prolonged syndrome: A report of two cases. J Neurosurg 1981;54:89-92. insertional activity and 1+ spontaneous activity), rectus femoris 8. Chu-Andrews J, Johnson R. Electrodiagnosis: an anatomical and (prolonged insertional activity and 2+ spontaneous activity), and clinical approach. Philadelphia: JB Lippincott; 1986. adductor longus (prolonged insertional activity and 1+ sponta- 9. Davidson MR. Heel neuroma: identification and removal. J Am neous activity). These muscles had normal motor unit recruit- Podiatry Assoc 1977;67:431-435. ment and MUAP morphology and amplitudes. The vastus 10. Daghino W, Pasquali M, Faletti C. Superficial peroneal nerve entrapment in a young athlete: the diagnostic contribution of magnetic medialis, tibialis anterior, tibialis posterior, flexor digitorum resonance imaging. J Foot Ankle Surg 1997;36:170-172. longus, gluteus medius, medial gastrocnemius, and first dorsal 11. Day FN 3rd, Naples JJ. Endoscopic tarsal tunnel release: update 96. interosseus pedis had no remarkable abnormalities. An attempt J Foot Ankle Surg 1996;35:225-229. was made to study the lumbosacral paraspinal muscles, but they 12. Delagi EF, Perotto A, Iazzetti J, Morrison D. Anatomic guide for the could not be reached with the longest needle available. electromyographer, 2nd edition. Springfield: Charles C. Thomas; 1980. 13. DeLisa JA, Lee HJ, Baran EM, Lai KS. Manual of nerve conduction Conclusions velocity and clinical neurophysiology, 3rd edition. New York: Raven Press; 1994. The EDX examination results showed evidence of right L3 14. Dellon AL. Deep peroneal nerve entrapment on the dorsum of the radiculopathy, which explained the low back pain and right foot. Foot Ankle 1990;11:73-80. thigh pain that improved with epidural steroid injection. Results 15. Dumitru D. Electrodiagnostic medicine. Philadelphia: Hanley & Belfus; 1995. also showed evidence of severe right ATTS, explaining the distal pain persisting in the right leg. AAEM Course Painful Foot and Ankle 7

16. Edlich HS, Fariss BL, Phillips VA, Chang DE, Smith JF, Hartigan C, 33. Lowdon IM. Superficial peroneal nerve entrapment. J Bone Joint Edlich RF. Talotibial exostoses with entrapment of the deep peroneal Surg Br 1985;67:58-59. nerve. J Emerg Med 1987;5:109-113. 34. Liu Z, Zhou J, Zhao L. Anterior tarsal tunnel syndrome. J Bone Joint 17. Eibel P. The anterior tarsal tunnel syndrome. J Bone Joint Surg Am Surg Br 1991;73:470-473. 1985;67:170. 35. McAuliffe TB, Fiddian NJ, Browett JP. Entrapment neuropathy of 18. Falck B, Alaranta H. Fibrillation potentials, positive sharp waves and the superficial peroneal nerve: a bilateral case. J Bone Joint Surg Br fasciculation in the intrinsic muscles of the foot in healthy subjects. J 1985;67:62-63. Neurol Neurosurg Psychiatry 1983;46:681-683. 36. Murphy PC, Baxter DE. Nerve entrapment of the foot and ankle in 19. Garfin S, Mubarak SJ, Owen CA. Exertional anterolateral-compart- runners. Clin Sports Med 1985;4:753-763. ment syndrome: case report with fascial defect, muscle herniation, 37. Oh SJ, Demirci M, Dajani B, Melo AC, Claussen GC. Distal sensory and superficial peroneal-nerve entrapment. J Bone Joint Surg Am nerve conduction of the superficial peroneal nerve: new method and 1977;59:404-405. its clinical application. Muscle Nerve 2001;24:689-694. 20. Gatens PF, Saeed MA. Electromyographic findings in the intrinsic 38. Ort L. Deep peroneal nerve entrapment: a case report. J Foot Surg muscles of normal feet. Arch Phys Med Rehabil 1982;63:317-318. 1973;12:20-21. 21. Geiringer SR. Anatomic localization for needle electromyography. 39. Piza-Katzer H, Pilz E. Compression syndrome of the superficial Philadelphia: Hanley & Belfus; 1994. fibular nerve. Case report. Handchir Mikrochir Plast Chir 22. Gessini L, Jandolo B, Pietrangeli A. The anterior tarsal tunnel syn- 1997;29:124-126. drome: report of four cases. J Bone Joint Surg Am 1984;66:786-787. 40. Reed SC, Wright CS. Compression of the deep branch of the per- 23. Horwitz MT. Normal anatomy and variations of the peripheral oneal nerve by the extensor hallucis brevis muscle: a variation of the nerves of the leg and foot. Arch Surg 1938;36:626-636. anterior tarsal tunnel syndrome. Can J Surg 1995;38:545-546. 24. Izzo KL, Sridhara CR, Rosenholtz H, Lemont H. Sensory conduc- 41. Sander HW. Mononeuropathy of the medial branch of the deep per- tion studies of the branches of the superficial peroneal nerve. Arch oneal nerve in a scuba diver. J Peripher Nerv Syst 1999;4:134-137. Phys Med Rehabil 1981;62:24-27. 42. Sarrafian SK. Anatomy of the foot and ankle. Philadelphia: JB 25. Kanbe K, Kubota H, Shirakura K, Hasegawa A, Udagawa E. Lippincott Co; 1983. Entrapment neuropathy of the deep peroneal nerve associated with 43. Sharma RR, Pawar SP, Dey P. An occult Schwannoma of the deep the extensor hallucis brevis. J Foot Ankle Surg 1995;34:560-562. peroneal nerve with neuralgia mimicking sciatica: case report and 26. Kernohan J, Levack B, Wilson JN. Entrapment of the superficial per- review of the literature. Ann Saudi Med 2000;20:57-59. oneal nerve: three case reports. J Bone Joint Surg Br 1985;67:60-61. 44. Sridhara CR, Izzo KL. Terminal sensory branches of the superficial 27. Knackfuss IG, Giordano V, Nogueira M, Giordano M. Compression peroneal nerve: An entrapment syndrome. Arch Phys Med Rehabil of the medial branch of the deep peroneal nerve, relieved by excision 1985;66:789-791. of an os intermetatarseum. A case report. Acta Orthop Belg 45. Styf J. Diagnosis of exercise-induced pain in the anterior aspect of the 2003;69:568-570. lower leg. Am J Sports Med 1988;16:165-169. 28. Kopell HP, Thompson WA. Peripheral entrapment neuropathies of 46. Styf J. Entrapment of the superficial peroneal nerve: diagnosis and the lower extremity. N Engl J Med 1960;262:56-60. results of decompression. J Bone Joint Surg Br 1989;71:131-135. 29. Krause KH, Witt T, Ross A. The anterior tarsal tunnel syndrome. J 47. Styf JR, Korner LM. Chronic anterior-compartment syndrome of the Neurol 1977;217:67-74. leg. J Bone Joint Surg Am 1986;68:1338-1347. 30. Kuritz HM. Anterior entrapment syndromes. J Foot Surg 48. van Dijk JG, van Benten I, Kramer CG, Stegeman DF. CMAP am- 1976;15:143-148. plitude cartography of muscles innervated by the median, ulnar, per- 31. Lawrence SJ, Botte MJ. The deep peroneal nerve in the foot and oneal, and tibial nerves. Muscle Nerve 1999;22:378-389. ankle: an anatomic study. Foot Ankle Int 1995;16:724-728. 49. Wiechers D, Guyton JD, Johnson EW. Electromyographic findings 32. Liveson JA, Ma DM. Laboratory reference for clinical neurophysiol- in the extensor digitorum brevis in a normal population. Arch Phys ogy. Philadelphia: FA Davis; 1992. Med Rehabil 1976;57:84-85. 8 AAEM Course 9

Baxter’s Nerve Entrapment

David R. Del Toro, MD Associate Professor Department of Physical Medicine and Rehabilitation Medical College of Wisconsin Milwaukee, Wisconsin

INTRODUCTION it was first described by Roegholt in 1940.28 Other terms in the literature include “nerve to the abductor digiti quinti,”3,16,23,27,32 The awareness and appreciation of the details of Baxter’s nerve and the “first branch of the lateral plantar nerve.”2,3,32,36 There entrapment in the foot requires that an electrodiagnostic (EDX) have been numerous citations in the orthope- consultant must first have a clear and accurate understanding of dic2,3,4,11,19,22,23,29,32,33,34 and podiatric1,27 literature reporting the tibial nerve and its branching pattern in the ankle and foot. Baxter’s nerve entrapment as a relatively common and treatable Therefore, this manuscript emphasizes that thorough knowledge cause of heel pain syndrome. The primary reason for distin- of the neuroanatomy of the foot and ankle is the fundamental guishing this nerve entrapment as being different from classic key to the EDX evaluation and subsequent diagnosis of focal TTS is the anatomic course of Baxter’s nerve, which is quite dis- neuropathies in the foot. Initial discussion will focus on Baxter’s similar, compared to the medial and lateral plantar nerves in the nerve and the relevant past literature regarding this nerve, fol- foot. The anatomic comparison between these tibial nerve lowed by the details of the neuroanatomy of the foot and ankle branches will be detailed in the next section of this article. particularly concentrating on the tibial nerve and its branches. Then the article will present details of the clinical presentation (including signs and symptoms) and the EDX evaluation, as it NEUROANATOMY pertains to Baxter’s nerve entrapment and in general, focal neuropathies in the foot. Finally, in the discussion the author stresses The tibial nerve has four terminal branches: the medial calcaneal the critical factors in distinguishing a focal Baxter’s neuropathy nerve (MCN); the medial plantar nerve (MPN); the lateral from other isolated neuropathies in the foot, particularly tarsal plantar nerve (LPN); and Baxter’s nerve (Figure 1). These tunnel syndrome (TTS), and offers a case report of Baxter’s branches are based on each nerve’s discrete anatomic course and nerve entrapment. different sites of entrapment within the foot. All of these tibial nerve branches pass through the proximal tarsal tunnel, but then their individual course begins to diverge. The MCN, believed to BACKGROUND be a purely sensory nerve, has a variable origin but relatively consistent terminal course and usually pierces the flexor retinaculum The term “Baxter’s nerve” is actually an informal name given to of the tarsal tunnel (Figure 1) to provide cutaneous innervation the nerve which ultimately innervates the abductor digiti quinti to the posterior, medial, and plantar surfaces of the heel (Figure pedis (ADQP) muscle in the foot. It is named for a famous or- 2).25,31 The different mechanisms of MCN entrapment include thopedic surgeon2,3,4 who has performed a large amount of clin- a tight fascial layer overlying the medial calcaneus,36 chronic ex- ical and research activity related to this nerve. The inferior ternal injury such as a patient’s shoe rubbing against a prominent calcaneal nerve was the initial formal name for Baxter’s nerve, as oscalcis, or possibly due to excessive pronation.36 In the lower 10 Baxter’s Nerve Entrapment AAEM Course

Figure 1 Medial aspect of a right foot. Note that Baxter’s nerve, usually the 1st branch off the LPN, in this case, branches off the tibial nerve, but still eventually lies deep to the AH. Also, the MCN branches pierce the FR as they course towards the medial/plantar aspect of the heel. (Adapted from Park T. and Del Toro D. Electrodiagnostic evaluation of the foot. Phys Med Rehabil Clin North Amer 1998;9:871-896, with permission.)

AH = abductor hallucis muscle; FR = flexor retinaculum; IFS = interfascicular septum; LPN = lateral plantar nerve; MCN = medial calcaneal nerve; MPN = medial plantar Figure 2 Cutaneous innervation of the plantar aspect of the foot. nerve; QP = quadratus plantae muscle; TN = tibial nerve. (Adapted from Sarrafian SK. Anatomy of the foot and ankle. Philadelphia: JB Lippincott Co; 1983, with permission.)

1 = medial calcaneal nerve; 2 = lateral calcaneal nerve; 3 = saphenous nerve; 4 = tarsal tunnel the interfascicular septum (IFS) is formed by the sural nerve; 5 = medial plantar nerve; 6 = lateral plantar nerve. deep fascia of the abductor hallucis muscle and this septum separates the MPN and LPN into the upper and lower calcaneal chambers, respectively. Both the MPN and LPN are mixed nerves that supply motor, cutaneous, articular, and vascular plantae and the overlying flexor digitorum brevis (Figure 3). branches in the foot. Along its proximal course, the nerve will usually give off pe- riosteal sensory branches to the medial calcaneal tuberosity,1,31 a In discussing the anatomic course of Baxter’s nerve, one must branch into the long plantar ligament and may send motor first realize that while it travels through the tarsal tunnel, it branches to the quadratus plantae and flexor digitorum brevis comes off distal to the MCN origin, and then within the lower (Figure 5).7,33 Finally, numerous anatomic dissection studies tarsal tunnel it usually branches off from the LPN (hence the have demonstrated that Baxter’s nerve always terminates with term 1st branch of the LPN) or sometimes off the tibial motor branches to the ADQP.1,4,7,9,27,29,33 Furthermore, of the nerve.1,3,4,7,10,16,21,27,29,31,33 After this branch point, Baxter’s nerve four terminal branches in the foot discussed above, Baxter’s then exits the posterior aspect of the lower calcaneal chamber, nerve is the only one not to have any cutaneous innervation. passing between the thick investing, taut deep fascia of the abductor hallucis (AH) (medially) and the quadratus plantae (laterally) (Figure 3).31 Next, at the level of the inferior border of the CLINICAL PRESENTATION AH deep fascia, Baxter’s nerve crosses laterally in nearly a transverse fashion immediately anterior to the medial calcaneal Since Baxter’s nerve has a distinct anatomic course as compared tuberosity (Figure 4) to pass between the underlying quadratus to the MPN and LPN in the foot, it has completely different AAEM Course Painful Foot and Ankle 11 sites of entrapment and consequently a somewhat different clin- removal of an anterior calcaneal heel spur. Additionally, it ical presentation. There are believed to be two major sites of en- has been postulated that this site could be clinically signifi- trapment of Baxter’s nerve after it leaves the tarsal tunnel: cant when there is inflammation of surrounding soft tissue structures (e.g., plantar fasciitis) since this would likely (1) The relatively unyielding space between the deep fascia of impact Baxter’s nerve due to its close proximity.1,36 the AH and the medial edge of the quadratus plantae which is the route which Baxter’s nerve follows (Figure 3).1,2,27,29 Clinically, Baxter’s nerve entrapment usually presents with the Baxter’s nerve may be particularly vulnerable at this site in a predominant symptom of chronic and constant medial/plantar pronated foot, since these two muscles are forced together heel pain,2,6,8 while infrequently it can be localized to the medial more firmly, consequently placing greater traction on this and lateral aspects of the heel.8 The pain can be described by nerve.33 various qualities, including sharp, dull, aching, throbbing, or burning and is often exacerbated by weight-bearing activities, (2) The anterior calcaneus and in particular the medial cal- such as prolonged walking and standing. The symptoms are pre- caneal tuberosity, especially if there is a heel spur present cipitated by sports in approximately 50% of cases2,8 and in the (Figure 4).2,23,27,36 Baxter’s nerve is believed to be vulnerable author’s clinical experience it can be preceded by a clinical course for entrapment at this site since it passes immediately in of plantar fasciitis. The heel pain in Baxter’s nerve entrapment front of the anterior calcaneus, with a mean distance differs, however, since it is often worse at night and is relatively between the medial calcaneal tuberosity and Baxter’s nerve constant (i.e., present at rest and with weight-bearing activities) of only 5.5 mm.1 Therefore, due to this intimate anatomic whereas in plantar fasciitis there is early morning heel pain that relationship, Baxter’s nerve may be injured during surgical can improve with subsequent stretching, the pain usually is not

Figure 3 Posterior view of the heel showing how Baxter’s nerve passes between the taut deep fascia of the abductor hallucis (medially) and the medial edge of the quadratus plantae (laterally). This is a potential site of entrapment for Baxter’s nerve since it is Figure 4 Anatomic course of Baxter’s nerve along the plantar particularly vulnerable to excessive traction with pronation. aspect of the heel. Note that Baxter’s nerve crosses immediately (Adapted from Schon L, Baxter D. Heel pain syndrome and entrap- anterior to the medial calcaneal tuberosity, near the origin of the ment neuropathies about the foot and ankle. In: Gould JS, plantar fascia and also the site for a possible heel spur. (Adapted Thompson FM, Cracchiolo C, editors. Operative foot surgery. from Baxter D, Pfeffer G, Thigpen M. Chronic heel pain: treatment Philadelphia, WB Saunders; 1994. p 192-208, with permission.) rationale. Orthop Clin 1989;20:563-569, with permission.) 12 Baxter’s Nerve Entrapment AAEM Course

Figure 5 Medial/plantar view of the foot showing the individual branches and eventual terminal course of Baxter’s nerve. Note that Baxter’s nerve, after sending nerve branches to the medial calcaneal tuberosity and the flexor digitorum brevis muscle, then terminates as nerve twigs supplying the ADQP muscle. (Adapted from Schon L, Baxter D. Heel pain syndrome and entrapment neuropathies about the foot and ankle. In: Gould JS, Thompson FM, Cracchiolo C, editors. Operative foot surgery. Philadelphia, WB Saunders; 1994. p 192-208, with permission.)

constant, and it can improve with rest (i.e., nonweight-bearing). pedis), and a Tinel sign over the anteromedial aspect of the Typically, with Baxter nerve entrapment, the patient does not heel.25,26 Notably, there are no cutaneous sensory deficits, and report any numbness or tingling in the foot, since Baxter’s nerve muscle stretch reflexes are normal.8,24,26 Plain radiographs has no cutaneous innervation, and generally, there is no signifi- demonstrate evidence of an anterior calcaneal heel spur in over cant complaint of weakness or gait problems. 50% of cases.6 The differential diagnosis should primarily include chronic plantar fasciitis, chronic heel pain syndrome, Physical examination usually demonstrates marked tenderness TTS, Achilles’ tendinitis/bursitis, medial calcaneal neuropathy, over the anteromedial aspect of the heel (or just in front of the lumbosacral (L-S) radiculopathy or plexopathy, peripheral medial aspect of the calcaneus).6 According to reports in the lit- polyneuropathy (especially if symptoms are bilateral), and other erature,15,33 the pathognomonic clinical sign of Baxter’s nerve en- conditions not listed here. trapment is greater pain with compression over the proximal medial aspect of the heel compared to the plantar aspect. This Most cases of Baxter’s nerve entrapment will resolve with con- maneuver should elicit the typical symptoms of burning, shoot- servative management, which includes nonsteroidal anti-inflam- ing, stabbing, tingling, electric, or sharp pain; sometimes there is matory drugs, shock-absorbing heel cups, a medial longitudinal radiation of the pain proximally and distally.33 Furthermore, it is arch support (for the excessively pronated foot), and local steroid proposed that palpation in this region pinches the nerve between injection.2,6 After approximately 6 months or more of conserva- the deep fascia of the AH and medial caudal margin of the quad- tive management, if the symptoms fail to resolve, surgical de- ratus plantae which results in the pain and possible paresthesia.2 compression may be indicated. Surgery usually involves release Other examination findings may include inability to abduct the of Baxter’s nerve between the AH and the quadratus plantae 5th toe, wasting or atrophy of the lateral aspect of the foot in the muscles (Figure 6). This surgical procedure usually includes in- region of the ADQP (also referred to as abductor digiti quinti cision of the taut deep fascia of the AH, a partial medial plantar AAEM Course Painful Foot and Ankle 13

ble for needle EMG examination, and because of their specific innervation pattern. A few studies have demonstrated abnormally prolonged insertional activity in intrinsic foot muscles in a considerable number of normal feet,13,14,37 and consequently, many EDX consultants will avoid performing the needle EMG examination in the foot because they are unsure on how to in- terpret these findings. However, these past studies have either failed to quantitate the observed abnormalities or they demonstrate that these abnormalities, when present, are quite mild.13,14,37 In fact, these studies recorded no actual abnormal spontaneous activity (in the form of sustained positive waves or fibrillation potentials) in any normal subjects. However, in a more recent study performed in an asymptomatic healthy population,12 a very low prevalence (i.e., 2% of the study popula- Figure 6 The surgical procedure performed for Baxter’s nerve en- tion) was found to have abnormal spontaneous activity, trapment includes incision of the deep fascia of the abductor hallu- specifically fibrillation potentials, in the intrinsic foot muscles cis. (Adapted from Schon L, Baxter D. Heel pain syndrome and studied.12 These results are consistent with this author’s extensive entrapment neuropathies about the foot and ankle. In: Gould JS, clinical experience in performing EDX studies in the foot. Thompson FM, Cracchiolo C, editors. Operative foot surgery. Therefore, in Baxter’s nerve entrapment, typical needle EMG Philadelphia, WB Saunders; 1994. p 192-208, with permission.) abnormalities would likely include evidence of partial denervation suggested by sustained fibrillation potentials or positive sharp waves and decreased motor unit recruitment noted only in fascia release, and a heel spur excision if necessary.2,15,23,27 the ADQP of the affected foot.8,24 Needle EMG examination of Following this procedure, 89% of patients report good or excel- other ipsilateral intrinsic foot muscles and the contralateral lent results.2 ADQP should be unremarkable. Consequently, this author con- siders, as well as others,20,35 that needle EMG examination of the intrinsic foot musculature is an essential component in the EDX ELECTRODIAGNOSTIC EVALUATION evaluation of the foot. Nerve conduction studies (NCSs) are also necessary in evaluating for Baxter’s nerve entrapment. However, Before discussing the specific details in the EDX evaluation of the motor NCS may not show any abnormalities with regards to Baxter’s nerve entrapment, there are several important concepts distal onset latency and amplitude (either baseline-to-peak or to consider. In order to perform a thorough needle electromyo- peak-to-peak), even when compared side-to-side. The reasons graphy (EMG) examination of intrinsic foot muscles, the EDX for this are likely multifactorial and include: consultant must learn to sample different muscles from different peripheral nerves within the foot (Table 1). (1) The tubular nature of the foot brings all the intrinsic foot muscles closer together physically and more parallel to one These muscles above are chosen frequently by the author due to another so it is more likely that a recorded compound their relatively superficial location, making them readily accessi- muscle action potential (CMAP) represents the summation

Table 1

Innervated by the Extensor digitorum brevis Deep peroneal nerve

4th dorsal interosseus pedis Lateral plantar nerve

Abductor hallucis Medial plantar nerve

Abductor digiti quinti pedis Baxter’s nerve 14 Baxter’s Nerve Entrapment AAEM Course

of potentials from several nearby muscles rather than a sum- mated potential dominated by one nearby muscle;

(2) Since nearly all the intrinsic muscles in the foot (except for extensor digitorum brevis [EDB]) are tibial innervated, these muscles are activated each time the tibial nerve is stim- ulated, thereby magnifying the problem described in 1;

(3) Because the tibial nerve and its branches (namely the MPN, LPN, and Baxter’s nerve) follow such a twisting course across the ankle and foot, any measurements that include these nerve branches are likely to be filled with error and un- certainty.

Nevertheless, the NCS is still an integral part in the EDX evaluation of the foot. Figure 7 Lateral view of the foot depicting two different E1 sites that were reportedly recording over the ADQP muscle. A, the E1 site With the above concepts in mind, the following information is proposed by Johnson and Ortiz.35 B, the E1 site proposed by Irani, a review of the EDX evaluation for a patient with suspected et al.36 Note that distally, most of the ADQP muscle is tendinous Baxter’s nerve entrapment. First, the needle EMG examination along the lateral aspect of the fifth metatarsal, while the FDMB should include the ADQP and other intrinsic foot muscles (such muscle belly is immediately deep to the ADQP tendon and inferior as 4th dorsal interosseus pedis, EDB, and AH) on the affected to the fifth metatarsal. ADQP=abductor digiti quinti pedis; side, more proximal leg muscles on the same side (e.g., tibialis FDMB=flexor digiti minimi brevis. (Adapted from Park T, Del Toro D. anterior, medial gastrocnemius, possibly tensor fascia lata and Electrodiagnostic evaluation of the foot. Phys Med Rehabil Clin lower L-S paraspinal) to exclude L-S radiculopathy or plexopa- North Am 1998;9:871-896, with permission.) thy, and possibly the ADQP on the unaffected side for comparison (principally for the inexperienced EDX consultant). Motor NCS should include Baxter’s nerve (recording over ADQP)9,18 bilaterally, MPN (recording over AH), and LPN (recording over there is a greater than 1.0 (or 1.5 ms) latency difference, or a flexor digiti minimi brevis [FDMB])9,17 on the affected side. To greater than 50% drop in amplitude. Electrodiagnostic consul- clarify the recording sites for the NCS technique for both tants should also realize that most of the time the Baxter’s nerve Baxter’s nerve and the LPN, the lateral plantar motor NCS uses CMAP (recording over the ADQP) has an initial downward de- an E1 site over the FDMB at the midpoint of the 5th metatarsal flection.9 The mixed NCS of both MPN and LPN30 should be on the lateral aspect of the foot according to a previously pub- performed on the affected foot, and if necessary on the unaf- lished technique,17 whereas Baxter’s NCS uses a different E1 site fected foot for comparison. Additionally, the MCN conduction which is over the ADQP inferior to the lateral malleolus (Figure technique25 could be performed if the clinical presentation sug- 7). Detailed electrophysiologic mapping of the ADQP CMAP gests involvement of the MCN. Finally, the NCS for the sural revealed that false motor points are common over the lateral nerve and the common peroneal motor nerve should be in- foot, but they are almost exclusively found anterior to the lateral cluded in the EDX evaluation in order to exclude a peripheral malleolus.9 For the NCS of Baxter’s nerve, the author’s recom- polyneuropathy. This is particularly important if the responses of mendation is to place the E1 electrode for the ADQP inferior the mixed NCS of the MPN and LPN are unobtainable or if the and slightly posterior to the tip of the lateral malleolus, approx- motor NCS of the tibial nerve branches reveal any abnormali- imately half-way between the tip of the lateral malleolus and the ties. sole of the foot similar to the technique previously mentioned18 Also, the parameters for Baxter’s NCS were published9 as follows: DISCUSSION

Mean onset latency (± 1 SD) = 4.4 (± 0.5 ms) Baxter’s nerve entrapment as a clinical entity and a etiology for heel pain has been well documented in the litera- Mean amplitude (± 1 SD) = 11.0 (± 3.9 mV) ture.1,2,3,4,8,11,19,22,23,27,29,32,33,34 Moreover, in a small case series by Del Toro and colleagues, two patients with heel pain were found This author becomes initially suspicious of an electrophysiologic to have EDX findings consistent with a focal Baxter’s nerve en- NCS finding if the absolute value is beyond two standard devi- trapment and were later confirmed by surgical outcome after un- ations of the mean value or using side-to-side comparison, if dergoing release of the nerve.8 Therefore, a focal Baxter’s AAEM Course Painful Foot and Ankle 15 neuropathy along with TTS should always be considered in the is likely a summation of potentials contributed from multiple differential diagnosis whenever an EDX consultant encounters a nearby intrinsic foot muscles, and not predominantly based on patient with foot pain (and particularly heel pain). Baxter’s nerve the ADQP, because of the anatomy of the foot. Consequently, in entrapment is distinct from TTS primarily due to the fact that the evaluation of focal foot neuropathies as with any EDX med- Baxter’s nerve has separate sites of entrapment in the foot as icine consultation, the EDX consultant, utilizing both the clini- compared to the MPN and LPN. The two principal sites of en- cal and electrophysiologic information, must use logical trapment of Baxter’s nerve in the foot are: (1) as it passes between diagnostic reasoning and internal consistency to deduce that the the taut deep fascia of the AH and the QP after exiting the tarsal “best fit” is the diagnosis of Baxter’s nerve entrapment. In con- tunnel (Figure 3) and (2) as it crosses the foot transversely, just clusion, the key components in the EDX evaluation of the foot immediately anterior to the medial calcaneal tuberosity and in diagnosing Baxter’s nerve entrapment are accurate knowl- (Figure 4) while eventually terminating with motor branches edge of the neuroanatomy of the foot and performing an appro- destined singularly for the ADQP. priate history and physical examination in conjunction with pertinent electrophysiologic data, obtained by a skilled EDX consultant. CASE REPORT

The following is a case report of a patient with Baxter’s nerve en- REFERENCES trapment.8 The patient was a 40-year-old white female with a one year history of left heel pain and plantar fasciitis. She de- 1. Arenson DJ, Cosentino GL, Suran SM. The inferior calcaneal nerve: scribed constant, sharp, throbbing pain over the medial and an anatomical study. J Am Podiatry Assoc 1980;70:552-560. 2. Baxter DE, Pfeffer GB. Treatment of chronic heel pain by surgical lateral aspect of the heel with symptoms exacerbated by weight- release of the first branch of the lateral plantar nerve. Clin Orthop bearing activities. She also reported nocturnal pain. She denied 1992;279:229-236. any numbness, tingling, or weakness in the left foot. Physical ex- 3. Baxter DE, Pfeffer GB, Thigpen M. Chronic heel pain: treatment ra- amination was remarkable for marked tenderness over the tionale. Orthop Clin 1989;20:563-569. medial and medial/plantar aspect (origin of plantar fascia) of the 4. Baxter DE, Thigpen CM. Heel pain—operative results. Foot Ankle left heel, Tinel sign present over the medial heel (paresthesia into 1984;5:16-25. 5. Davidson MR, Copoloff JA. Neuromas of the heel. Clin Podiatr Med 4th and 5th toes). There was no sensory deficit nor weakness Surg 1990;7:271-288. noted in the left foot, and ankle, and muscle stretch reflexes were 6. Davis PF, Severud E, Baxter DE. Painful heel syndrome: Results of symmetric in both legs. Electrodiagnostic studies revealed needle nonoperative treatment. Foot Ankle Int 1994;15:531-535. EMG findings of 2+ fibrillation potentials and positive sharp 7. del Sol M, Olave E, Gabrielli C, Mandiola E, Prates JC. Innervation waves noted only in the left ADQP but no EMG abnormalities of the abductor digiti minimi muscle of the human foot: anatomical basis of the entrapment of the abductor digiti minimi nerve. Surg in the other intrinsic left foot muscles or the right ADQP. Also, Radiol Anat 2002;24:18-22. NCSs were normal for Baxter’s nerve bilaterally, and for both 8. Del Toro, D., R. Dei, and T. Marquardt, Electrodiagnostic Findings medial and lateral plantar nerves (motor and mixed NCS) in the and Surgical Outcome in Isolated 1st Branch Lateral Plantar left foot. Based on the patient’s clinical presentation in conjunc- Neuropathy: A Case Series. Arch Phys Med Rehabil, 2002. 83(11): tion with the electrophysiologic results, the EDX impression was p. 1657. given as a focal Baxter’s neuropathy. After conservative manage- 9. Del Toro DR, Mazur A, Dwzierzynski WW, Park TA. Electrophysiologic mapping and cadaveric dissection of the lateral ment failed, she underwent surgical decompression of Baxter’s foot: Implications for tibial motor nerve conduction studies. Arch nerve which included release of the deep fascia of the AH and a Phys Med Rehabil 1998;79:823-826. partial release of the plantar fascia. At follow-up 10 months after 10. Didia BC, Horsefall AU. Medial calcaneal nerve: An anatomical surgery, the patient reported no heel pain as her prior symptoms study. J Am Podiatr Med Assoc 1990;80:115-119. and the Baxter’s nerve entrapment were essentially resolved. 11. Dreeben S, Mann R. Heel pain: sorting through the differential diagnosis. J Musculoskel Med 1992;9:21-37. 12. Dumitru D, Diaz CA, King JC. Prevalence of denervation in paraspinal and foot intrinsic musculature. Am J Phys Med Rehabil SUMMARY 2001;80:482-490. 13. Falck B, Alaranta H. Fibrillation potentials, positive sharp waves and In the author’s clinical experience with EDX evaluation of focal fasciculation in the intrinsic muscles of the foot in healthy subjects. J neuropathies in the foot, the incidence of Baxter’s nerve entrap- Neurol Neurosurg Psychiatry 1983;46:681-683. 14. Gatens P, Saeed M. Electromyographic findings in the intrinsic ment is much higher than that of TTS. Empirically, the author muscles of normal feet. Arch Phys Med Rehabil 1982;63:317-318. has found that in cases of “positive” Baxter’s neuropathy the fre- 15. Goecker RM, Banks AS. Analysis of release of the first branch of the quency of abnormal needle EMG findings is much higher as lateral plantar nerve. J Am Podiatr Med Assoc 2000;90:281-286. compared to abnormal NCS results. One possible explanation 16. Hamm J, Sanders M. Anatomic variations of the nerve to the abduc- for this is that the Baxter’s nerve CMAP (recording over ADQP) tor digiti quinti muscle. Foot Ankle 1987;8:123. 16 Baxter’s Nerve Entrapment AAEM Course

17. Irani KD, Grabois M, Harvey SC. Standardized technique for diag- 29. Rondhuis JJ, Huson A. The first branch of the lateral plantar nerve nosis of tarsal tunnel syndrome. Am J Phys Med 1982;61:26-31. and heel pain. Acta Morphol Neerl Scand 1986;24:269-279. 18. Johnson EW, Ortiz PR. Electrodiagnosis of tarsal tunnel syndrome. 30. Saeed M, Gatens P. Compound nerve action potentials of the medial Arch Phys Med Rehabil 1996;47:776-780. and lateral plantar nerves through the tarsal tunnel. Arch Phys Med 19. Kenzora JE. The painful heel syndrome: an entrapment neuropathy. Rehabil 1982;63:304-307. Bull Hosp Jt Dis Orthop Inst 1987;47:178-189. 31. Sarrafian SK. Anatomy of the foot and ankle. Philadelphia: JB 20. Kraft G. Tarsal tunnel entrapment. In: 1986 AAEE Course E: Lippincott; 1983. Entrapment neuropathies. Rochester, MN: American Association of 32. Schon L, Baxter D. Neuropathies of the foot and ankle in athletes. Electrodiagnostic Medicine; 1986. p 13-18. Clin Sports Med 1990;9:489-509. 21. Louisia S, Masquelet AC. The medial and inferior calcaneal nerves: 33. Schon L, Baxter D. Heel pain syndrome and entrapment neu- an anatomic study. Surg Radiol Anat 1999;21:169-173. ropathies about the foot and ankle. In: Gould JS, Thompson FM, 22. Lutter LD. Surgical decisions in athletes’ subcalcaneal pain. Am J Cracchiolo C, editors. Operative foot surgery. Philadelphia: WB Sports Med 1986;14:481-485. Saunders; 1994. p 192-208. 23. Murphy PC, Baxter DE. Nerve entrapment of the foot and ankle in 34. Schon LC, Glennon TP, Baxter DE. Heel pain syndrome: electrodi- runners. Clin Sports Med 1985;4:753-763. agnostic support for nerve entrapment. Foot Ankle 1993;14:129- 24. Park T, Del Toro D. Isolated inferior calcaneal neuropathy. Muscle 135. Nerve 1996;19:106-108. 35. Spindler HA, Reischer MA, Felsenthal G. Electrodiagnostic assess- 25. Park T, Del Toro D. The medial calcaneal nerve: anatomy and nerve ment in suspected tarsal tunnel syndrome. Phys Med Rehabil Clin conduction technique. Muscle Nerve 1995;18:32-38. North Am 1994;5:595-612. 26. Pfeffer G. Plantar heel pain. In: Baxter DE, editor. The foot and ankle 36. Tanz SS. Heel pain. Clin Orthop 1963;28:169-178. in sport. St. Louis: Mosby-Year Book; 1995. 37. Wiechers D, Guyton JD, Johnson EW. Electromyographic findings 27. Przylucki H, Jones CL. Entrapment neuropathy of muscle branch of in the extensor digitorum brevis in a normal population. Arch Phys lateral plantar nerve: a case of heel pain. J Amer Podiatry Assoc Med Rehabil 1976;57:84-85. 1981;71:119-124. 28. Roegholt MN. Een nervus calcaneus inferior als overbrenger van de pijn bij calcaneodynie of calcanensspoor en de daaruit volgende ther- apie. Ned Tijdschr v Geneeskd 1940;84:1898. 17

Tarsal Tunnel Syndrome

Mohammad A. Saeed, MD, MS Clinical Associate Professor Department of Rehabilitation Medicine University of Washington School of Medicine

INTRODUCTION (laciniate ligament). The floor consists of the medial surface of the talus, the sustentacum tali, and the medial wall of the calca- Tarsal tunnel syndrome (TTS) is an entrapment neuropathy of neus. The superior border is formed by the superficial and deep the tibial nerve or its terminal branches at the ankle within the aponeurotic fascia of the leg and the inferior border by the ab- fibro-osseous tunnel as it travels deep to the flexor retinaculum. ductor hallucis muscle. Individual fibrous septae extend from Keck and Lam first described TTS independently in 1962. the inner surface of the flexor retinaculum to the periosteum of There have been extensive publications on this topic, but con- the calcaneus. Within these septae, besides the tibial nerve, run troversies still exist, although there have been many advances in the posterior tibial artery and vein, and the tendons of the tib- the understanding of the anatomy, pathophysiology, diagnosis, ialis posterior, flexor digitorum longus, and flexor hallucis and treatment of TTS and other distal tibial neuropathies. Tarsal muscles. The tibial nerve branches into the medial plantar nerve tunnel syndrome is the most common entrapment neuropathy (MPN), lateral plantar nerve (LPN), and medial calcaneal nerve of the tibial nerve, but it is relatively uncommon. Although exact (MCN), usually within the confines of the tarsal tunnel proper. incidence is not known, it does depend on how hard someone Baxter’s nerve (also called the “inferior calcaneal nerve,” the “first looks for it. In this author’s experience the incidence is about branch of the LPN,” the “muscle branch of the LPN,” and the 0.6%.27 This correlates well with the study of Oh and colleagues “nerve to the abductor digiti quinti”) commonly branches from who reported incidence of 0.5%.20 the LPN, although it may come off the tibial nerve as a separate branch in up to 46% of the feet.21 In over 90% of the population, the branching of the tibial nerve into the MPN and LPN ANATOMY occurs within the tarsal tunnel region (Figure 1a).

In contrast to the carpal tunnel, the tarsal tunnel has a thinner The MPN is a mixed nerve, providing sensory innervation to the flexor retinaculum and contains—not just the tibial nerve—but medial aspect of the sole and to the plantar aspect of the 1st, the posterior tibial artery and vein. (No vessels accompany the 2nd, 3rd, and medial half of the 4th toes. Its motor fibers inner- median nerve through the carpal tunnel.) vate the abductor hallucis, flexor hallucis brevis, flexor digitorum brevis, and 1st lumbrical. The tarsal tunnel extends from the distal tibia to the plantar aspect of the navicular and may be divided at the talus into the The LPN is also a mixed nerve. Its sensory fibers provide cuta- upper (tibiotalar) tunnel and the lower (talocalcaneal) tunnel.21 neous innervation to the lateral aspect of the sole, and to the The roof of the tarsal tunnel is formed by the flexor retinaculum plantar aspect of the 5th and lateral half of the 4th toes. Its motor 18 Tarsal Tunnel Syndrome AAEM Course

consists of entrapment of the tibial nerve in the retromalleolar region, (or at the proximal end of the tunnel with corresponding clinical symptoms). Distal TTS involves one or more terminal branches of the tibial nerve, such as the MPN, LPN, MCN, or Baxter’s nerve23,26 An electrodiagnostic approach to TTS must consider the fact that pathology can occur in either area. Localized pathology may involve only one of these nerves or branches (Figures 1a and 1b).

ETIOLOGY OF TARSAL TUNNEL SYNDROME

A number of causes have been reported in the literature for TTS, and these have been classified into five broad categories: (1) traumatic; (2) compressive (by space-occupying lesions); (3) sys- Figure 1a Tibial nerve beneath the flexor retinaculum. temic; (4) biomechanical; and (5) idiopathic.4

AH = abductor hallucis; MPN = medial plantar nerve; IFS = inter fascicular septum; The most common cause of TTS is trauma, which accounts for 15 TN = tibal nerve; FR = flexor retinaculum; LPN = lateral plantar nerve; INC = inferior the majority of these cases. Cumulative trauma (micro-trauma) calcaneal nerve; MCN = medial calcaneal nerve can be a factor in some cases. Trauma may include fractures of the ankle and foot, ankle sprains, and surgical procedures around the foot and ankle. Some of the other etiological factors are innervation includes the quadratus plantae, flexor digiti minimi space-occupying lesions, such as ganglia, anomalous or hyper- brevis, flexor hallucis brevis (lateral head), adductor hallucis, all trophied muscles, neurilemoma, schwannoma, tenosynovitis, interossei, and 2nd, 3rd, and 4th lumbricals. and chronic thrombophlebitis. Systemic causes include hyper- lipidemia, gout, hypothyroidism, acromegaly, rheumatoid Baxter’s nerve innervates the abductor digiti minimi pedis arthritis, varicosities, and diabetes mellitus. Biomechanical (ADMP). It may sometimes send motor branches to the quad- causes include tarsal joint impaction due to hypermobility of the ratus plantae and flexor digitorum brevis as well. It provides no first ray, rigid joint structures, tarsal joint coalition and rearfoot cutaneous innervation in the foot. varus.4 As in carpal tunnel syndrome, the cause of TTS in some cases is unknown.18 The MCN is a purely sensory branch and provides cutaneous innervation to the posterior, medial, and plantar surfaces of the heel. The MCN has a highly variable course. It usually originates from the tibial nerve but may also come from the LPN or from the MPN/LPN bifurcation. When originating in the tarsal tunnel, the MCN must pierce the flexor retinaculum on its way to the medial and plantar surfaces of the calcaneal region.22

In the lower tarsal tunnel at the level of calcaneus, the tunnel for the tibial nerve is divided by the interfascicular septum into the upper and lower calcaneal chambers. The deep fascia of the abductor hallucis forms the interfascicular septum when this fascia extends towards its attachments to the medial aspect of the calcaneus. The MPN travels within the upper chamber and the LPN travels within the lower chamber. The MPN or LPN can be entrapped through the calcaneal chambers by the proximal or distal edge of the interfascicular septum.21 Figure 1b Medial and lateral plantar nerves penetrating the fibrous origin of the abductor hallucis and its branches (portapedis The tarsal tunnel can be divided into the proximal tarsal tunnel area). and the distal tarsal tunnel (or porta pedis).5,11,23 Proximal TTS AAEM Course Painful Foot and Ankle 19

CLINICAL FINDINGS

Typical symptoms include burning pain and paresthesia of the toes and sole of the feet. Classically the symptoms are worse at night, increased by activity and diminished with rest. There may also be numbness on the plantar aspect of the foot involving one or more of the tibial nerve branches. The most helpful diagnostic criteria are a positive Tinel sign at the proximal or distal tarsal tunnel area (sometimes accompanied by tingling discomfort radiating proximally along the nerve, a finding known as the Valleix phenomenon)4,15 and objective sensory loss in the territory of any of the terminal branches of the tibial nerve. Forcing the heel into maximum inversion or eversion may aggravate the symptoms. It should be noted, however, that not all four branches are affected in all cases. Weakness of toe flexion and atrophy of the intrinsic foot muscles are rare. Detecting weakness of toe flexion and intrinsic foot muscles can be difficult. Calcaneal branches are often spared, and thus, the heel pad usually has normal sensation. Bilateral TTS is relatively rare and for bilateral neuritic symptoms, it is important to rule out generalized peripheral neuropathy.

ELECTRODIAGNOSTIC EVALUATION

Electrodiagnostic studies should be performed on all patients suspected of having TTS. Motor, sensory, and mixed nerve conduction studies (NCSs) as well as needle EMG can assist in confirming the diagnosis of TTS in over 90% of cases.17,18 Motor NCSs of the tibial nerve are not as helpful because of low sensitivity. Prolonged terminal latency of the tibial nerve was observed in 47% of the cases.17 In one series, near-nerve sensory NCS of the MPN and LPN were abnormal in more than 90% of the cases.19 The MPN, LPN, and Baxter’s nerve should always be tested, because only one may be affected in some cases.

Placing an active recording electrode over the abductor hallucis Figure 2 Recording sites for MPN, ICN (Baxter’s nerve), and LPN no more than 1 cm inferior and 1 cm posterior to the navicular CMAPs. tuberosity is most commonly used for the MPN motor NCS. 1,21 This will avoid recording from a false motor point. The LPN ADMP= abductor digiti minimi pedis; CMAP = compound muscle action potential; motor NCS is commonly performed by placing an active FDMB = flexor digiti minimi brevis; ICN = inferior calcaneal nerve; LPN = lateral recording electrode over the ADMP. Irani and Grabois12 pro- plantar nerve; MPN = medial plantar nerve. posed recording at the mid-point of the fifth metatarsal, and Johnson and Ortiz13 suggested a recording site inferior to the lateral malleolus (Figure 2). According to Park and Del Toro,21 lateral malleolus.21 The stimulation site for all three is the medial the bulkiest portion of the ADMP belly is located just inferior to ankle, posterior to the tibia and just proximal to the medial the lateral malleollus, but the muscle becomes entirely tendinous malleolus. by the time it reaches the midpoint of the fifth metatarsal. Immediately underneath this tendon is the flexor digiti minimi Felsenthal and colleagues described a technique of motor NCS brevis (FDMB) (Figure 2). It also appears that the ADMP is of the tibial nerve across the tarsal tunnel7 (Figure 3). It estab- always innervated by Baxter’s nerve and the FDMB is always in- lished both a distal latency across the abductor tunnel as well as nervated by the LPN. Park and Del Toro21 proposed a recording proximal latency across the tarsal tunnel. Abnormalities could be site for the LPN over the FDMB at the mid point of the fifth diagnosed using the decrement of the amplitude across the tarsal metatarsal, and for Baxter’s nerve over the ADMP inferior to the tunnel or abnormal latency across the tarsal tunnel (Table 1). 20 Tarsal Tunnel Syndrome AAEM Course

It is generally agreed that the most sensitive test for possible compromise of the MPN, LPN, or tibial nerve is some form of sensory NCSs.4 There are two methods for performing pure sensory NCSs of the plantar nerves: one using the surface recording electrodes20 and the other near-nerve needle elec- trodes19 (Figure 4). Pure sensory potentials can be recorded by stimulating the first and fifth digits and recording from the tibial nerve proximal to the flexor retinaculum (orthodromic technique) or by stimulating the tibial nerve and recording from the first and fifth digits (antidromic technique).25 Responses recorded with these techniques are generally small, even with extensive signal averaging. Sensory nerve action potential (SNAP) studies have two main disadvantages: (1) they are time consuming and unpleasant for some patients, and (2) there may be no SNAPs in some normal subjects. In this author’s experience even with averaging, pure sensory responses are difficult to obtain in healthy subjects. Gelardi and colleagues also found no plantar sensory responses in 8% of the normal subjects.9 The near-nerve techniques can be quite time consuming and uncomfortable for the patient. However, this is the only viable technique for electrodiagnostic evaluation of interdigital neuropathy (Table 2, normal values).25

Saeed and Gaten described a technique for mixed NCSs of the MPN and LPN24 (Figure 5). This method records the mixed nerve action potential from the tibial nerve with a bar electrode placed behind the medial malleolus. Electrical stimulation is applied to the plantar aspect of the foot over the MPN or LPN at a 14 cm distance to the recording electrode. Saeed and Gaten found the mixed nerve conduction studies for MPN and LPN, which predominantly test the sensory fibers, to be more practi- cal and clinically useful because it can be performed quickly and easily. However, in patients with thick calluses it can be difficult to stimulate the MPN and LPN on the plantar surface of the foot. Ankle edema or swelling may cause difficulty with recording the response and may require recording with needle electrodes. In older patients (especially those over the age of 70), if the responses are absent on both sides, interpretation should be done with caution. Despite these technical difficulties, mixed NCSs of the MPN and LPN are the most easily performed and reliable techniques available.

Many prefer the Saeed and Gatens technique because it is easy and has the advantage of not requiring a signal average. Galardi and colleagues in 2000, reported their findings after comparing motor, orthodromic sensory, and mixed NCSs for the MPN Figure 3 Motor nerve conduction of the tibial nerve across tarsal and LPN in patients with TTS.9 They found the sensory and tunnel. mixed NCSs to be much more sensitive than the motor NCSs. Although mixed NCSs are less sensitive, they are more specific ADQ = abductor digiti quinti; FHL = flexor hallucis longus; R1 = recording active elec- than sensory NCSs. The recommended mixed NCSs because of trode over the flexor hallucis brevis; R2 = recording active electrode over the flexor the decreased likelihood of false positive results, especially for digiti minimi brevis; S1 = distal stimulating electrode; S2 = proximal stimulating pre-surgical diagnosis of TTS. electrode. AAEM Course Painful Foot and Ankle 21

Table 1 NORMAL DATA: Number of subjects: 32. Age range: 20-45 years.

Medial Plantar Nerve Lateral Plantar Nerve

Normal Normal Measurement Mean ± SD Limit Mean ± SD Limit

Latency Distal (ms) 4.5 ± 0.7 5.9 4.5 ± 0.7 5.9 Proximal (ms) 6.9 ± 0.8 8.5 6.9 ± 0.7 8.3 Across tarsal tunnel (ms) 2.4 ± 0.4 3.2 2.4 ± 0.4 3.2 Side-to-side difference 0.9 0.9 Amplitude Distal (mV) 7.7 ± 3.6 1.7 12.0 ± 05.6 3.0 Proximal (mV) 6.9 ± 3.3 2.4 10.8 ± 05.3 3.0 Across tarsal tunnel (%) 10.3 ± 9.0 27.6 10.2 ± 8.5 26.05 NCV (m/s) 49.4 ± 5.3 38.8 50.9 ± 5.2 40.7 INTERPRETATION: An amplitude decrement of more than 30% across the tarsal tunnel is considered abnormal. A side-to-side variation of more than 50% of the amplitude is unusual.

SD = standard deviation; NCV = nerve conduction velocity. Felsenthal’s Method (motor NCS of the tibial nerve across tarsal tunnel)

Needle electrode examination of intrinsic foot muscles is impor- tunnel with tibial NCV to the knee. Motor NCSs across the tant but often underutilized. Additional training in proper tech- tarsal tunnel may be helpful in locating the lesion proximal or nique and comfort is often lacking. The use of ethyl chloride distal to the inferior margin of the flexor retinaculum;7 (2) sural spray can reduce the discomfort experienced by some patients on and superficial peroneal sensory NCS on at least one side; (3) H- needle insertion, as can using the smallest needle electrodes avail- reflex studies, especially in the case of bilateral symptoms; (4) able. The needle EMG examination for screening of TTS should needle EMG of the intrinsic foot muscles and limited lower ex- include at least one muscle supplied by each of the motor tremity screening, including lumbosacral paraspinal muscles if branches of the tibial nerve; use abductor hallucis for the MPN, indicated; and (5) near-nerve recording, if necessary to obtain the fourth dorsal interosseus for the LPN, and the ADMP for sensory responses. Baxter’s nerve. The needle examination may show denervation in the involved intrinsic muscles of the foot depending on the The MPN or LPN can be entrapped through the calcaneal degree of secondary axonal degeneration and the nerves in- chambers by the proximal or distal edge of the interfascicular volved. Motor unit recruitment of intrinsic foot muscles can be septum. Symptoms may be in the distribution of MPN, LPN, difficult to evaluate. It is always prudent to compare the needle or both depending upon which nerve is involved. There may be EMG findings with those of the asymptomatic foot.10 If abnor- vague pain on the medial side of the foot. A positive Tinel’s sign malities are present in all these muscles, EDB (peroneal inner- may be present at the exit point of the tarsal tunnel or along the vated muscle) should also be included to verify that the length of the interfascicular septum to its distal edge just proxi- abnormalities are not limited to the tibial nerve distribution and mal to the abductor canal. may be due to a generalized process or peripheral neuropathy. In this author’s experience, a significant amount of membrane in- Nerve conduction studies may demonstrate both prolonged la- stability is not present in normal persons. tencies, or small motor, sensory, or mixed nerve responses in the affected nerve with no abnormality seen in other tibial nerve In clinical practice, when TTS is suspected, electrophysiological branches. Needle EMG examination will be abnormal in the in- evaluation should include the following: (1) bilateral MPN and trinsic foot muscles supplied by the affected nerve only. Despite LPN motor NCS and sensory or mixed NCS across the tarsal refinements in electrodiagnostic techniques, it can be difficult to 22 Tarsal Tunnel Syndrome AAEM Course

Figure 4a Sensory nerve conduction study of the plantar nerves

Figure 4b Interdigital nerve conduction study of the foot

diagnose true TTS or to distinguish it from other focal or gen- abductor tunnel. Nerve conduction studies and needle EMG eralized neuropathies (Table 3). examinations demonstrate abnormalities similar to those seen with MPN entrapment by the interfascicular septum.21

MEDIAL PLANTAR NEUROPATHY IN THE ABDUCTOR CANAL LATERAL PLANTAR NEUROPATHY IN THE ABDUCTOR CANAL The MPN can be compressed in isolation along its pathway distal to the tarsal tunnel. The common site of compression is at The LPN can be compressed along its pathway distal to the the abductor tunnel (the fibromuscular tunnel) behind the nav- tarsal tunnel, causing a lateral plantar neuropathy. Sensory loss is icular tuberosity (Figure 1). Reversible medial plantar neuropa- confined to the lateral sole. Nerve conduction studies and needle thy among joggers (jogger’s foot) has been described.21 EMG examinations demonstrate abnormalities similar to those Apparently, prolonged running with a valgus running style pro- seen with LPN entrapment by the interfascicular septum.21 duces repeated injury to the MPN at the abductor tunnel. Terminal latency to the FDMB muscle may be prolonged and the Clinically, these patients have burning or tingling over the compound muscle action potential may be small. Mixed or sensory medial sole and tenderness over the MPN at its entrance to the LPN latencies may be prolonged, or the response abnormal or AAEM Course Painful Foot and Ankle 23

Table 2 Normal values (Normal Limit) of tibial nerve and plantar nerve conduction*

Latency (ms) Amplitude NCV (m/s) (mV/µV) Onset** Negative peak***

TIBIAL NERVE Motor NCS of Tibial Nerve;17 Terminal latency (10cm) 5.1 5.0 NCV 40.6 Motor NCS of Plantar Nerve:2 Medial (8 cm) AHB 4.4 5.0 Lateral (ICN) (8 cm) ADQP 4.6 3.0 Medial (10 cm) AHB 4.8 5.0 Lateral (ICN) (10 cm) ADQP 4.9 3.0 Lateral (20 cm) FDMB 7.8 3.0 Mixed NCS of Plantar Nerve:21 Medial (14cm) 3.7 5.0 Lateral (14cm) 3.7 3.0 Sensory NCS of Medial Calcaneal Nerve:21 Latency 2.1 2.8 8.0 Sensory NCS of Plantar Nerve with the Surface E1ectrodes:17 Medial 28.0 2.0 Lateral 22.9 1.0 Sensory NCS of the Interdigital Nerves with the Near-Nerve Needle Recording17, 19 I 35.1/35.8* 30.3/28.5 2.7/1.3 V 30.4/24.6 25.9/21.6 0.7/0.4

ADQP = abductor digiti quinti pedis; AHB = abductor hallucis brevis; FDMB = flexor digiti minimi brevis; ICN = inferior calcaneal nerve; NCS = nerve conduction study; NCV = nerve conduction velocity. * Normal values for 20-49 yr/Normal values for 50-59 yr. **Onset of the initial deflection of potentials. *** Peak of the negative deflection of potentials.

absent.3 Needle EMG may show signs of denervation in the usually small and difficult to obtain in some normal individuals. FDMB and dorsal interosseous muscles. Its clinical usefulness is still questionable.

MEDIAL CALCANEAL NEUROPATHY DIFFERENTIAL DIAGNOSIS

Medial calcaneal neuropathy (MCN) often presents pain and Electrodiagnostic evaluation is very important in defining the paresthesias along the medial aspect of the heel without any presence or absence of neuropathic disorders (Table 3). Distal weakness. The pain tends to worsen with ambulation. It is mononeuropathies, such as medial or lateral plantar neu- common to have local tenderness or a Tinel’s sign over the MCN ropathies and proximal nerve lesions like sciatic or tibial neu- and numbness and tingling over the medial side of the heel. ropathy in the popliteal fossa and thigh, can mimic TTS. In Diagnosis of MCN neuropathy can be confirmed by NCS of the cases of sciatic or proximal tibial neuropathy, there will be an ab- MCN.22 This should include side-to-side comparison of the normal sural NCS and an abnormal needle EMG of the tibial- MCN SNAP amplitude and latency. The MCN response is innervated muscles proximal to the ankle. L5 or S1 24 Tarsal Tunnel Syndrome AAEM Course

Figure 5 Mixed nerve conduction studies of the medial and lateral plantar nerves.

radiculopathy can be present with symptoms limited to the sole TREATMENT of the foot, but a needle examination may reveal abnormalities in L5 or S1 innervated muscles proximal to the foot, and—in The treatment of TTS depends on the cause, and this can be the case of S1 nerve root compromise—the H-reflex study will classified into non-operative and operative. If there is no struc- be abnormal. Ischemic monomelic neuropathy, a disorder char- tural abnormality present, then it is appropriate to begin with acterized by acute onset burning pain in the foot or toes result- conservative treatment removing aggravating factors, such as ing from arterial occlusion usually between the hips and knees, poorly-fitting shoes, or applying corrective foot orthosis. may be confused with TTS.16 Certain musculoskeletal disorders can simulate TTS. Plantar fasciitis may present with similar symptoms. However, plantar fasciitis characteristically causes NONOPERATIVE TREATMENT foot pain when first standing up in the morning, localized at the origin of the plantar fascia at the calcaneus, whereas TTS tends Nonsteroidal anti-inflammatory drugs and corticosteroid injec- to produce medial heel and arch pain along the abductor hallu- tions are most helpful in the presence of tenosynovitis and in- cis muscle and sensory symptoms. Plantar fasciitis is associated flammatory arthropathies, such as rheumatoid arthritis or with localized tenderness, but nocturnal paresthias are more ankylosing spondylitis. Care must be taken to avoid direct injec- common with TTS. Foot pain may also be due to orthopedic tion into the tibialis posterior tendon. Other non-operative causes such as collapsed metatarsal heads or longitudinal arch treatments include pressure stocking to decrease swelling and sprain and rheumatological disorders such as ankylosing venous stasis, and weight loss for obese patients. In patients who spondylitis or gout. Electrodiagnostic studies are typically have symptoms reproduced by dorsiflexion, a heel lift may normal if the foot symptoms are due to these musculoskeletal relieve symptoms by decreasing tension on the tibial nerve. causes. Runners with hyperpronated feet may benefit from a slightly toe-in foot-strike to shift pressure to the lateral aspect of the foot, Plain radiograph examination of the foot can identify displaced thus decreasing stretch on the tibial nerve. fractures, accessory ossicles and bony exostoses within the vicin- ity of the tarsal tunnel. Weight-bearing radiographs may demon- Nonoperative treatment is most effective for the patient with strate foot deformities. tenosynovitis or flexible foot deformities.

Magnetic resonance imaging (MRI) is effective for assessing the contents of the tarsal tunnel and the branches of the tibial OPERATIVE TREATMENT nerve.6,8 It is especially useful in post-traumatic cases and space- occupying lesions. In cases of failed tarsal tunnel release, MRI is When the conservative approach fails, then surgical exploration recommended to assess the neural and surrounding structures.14 of the tibial nerve or its branches in the foot may be necessary. Ultrasound may be of value in some cases. Nerve compression within the tarsal tunnel in the presence of a AAEM Course Painful Foot and Ankle 25

Table 3 Differential diagnosis of tarsal tunnel syndrome Table 4 Motor nerve conduction of the posterior tibial nerve (Felsenthal’s technique) 1. Proximal or “true” tarsal tunnel syndrome (TTS) 2. Medial plantar neuropathy in the distal tarsal tunnel or abductor canal Distal Proximal Across- tunnel 3. Lateral plantar neuropathy in the distal tarsal tunnel or abductor canal Left Medial Plantar Motor Latency 3.3 ms 5.5 ms 2.2 ms

4. Chronic compressive medial and/or lateral plantar neuropathy Right Medial Plantar Motor Latency 3.2 ms 6.4 ms 3.2 ms 5. Medial calcaneal neuropathy Left Lateral Plantar Motor Latency 3.3 ms 5.6 ms 2.5 ms 6. Baxter’s neuropathy (or inferior calcaneal neuropathy) 7. Generalized peripheral neuropathy Right Lateral Plantar Motor Latency 3.3 ms 6.9 ms 3.6 ms 8. Distal tibial neuropathy secondary to, or TTS complicated by, Right Posterior Tibial Motor NCV = 46 M/S generalized peripheral neuropathy 9. Proximal tibial neuropathy 10. Sciatic neuropathy, lumbosacral plexopathy, or radiculopathy 11. Musculo-ligamentous: plantar fasciitis, soft tissue sprains/strains, aspect of right foot. He has a history of a fall onto his out- tenosynovitis, and bursitis stretched arm with injury to wrist and right ankle. A physical examination showed tenderness over the right tarsal tunnel region. Sensory examination revealed decreased sensation in the plantar aspect of the right foot. Otherwise right lower extremity space-occupying lesion is an indication for surgical decompres- examination was unremarkable. sion. However, in the absence of any space-occupying lesion or focal compression of the tibial nerve, tarsal tunnel release must Results of EDX studies of the plantar motor and mixed nerves be carefully considered. are given in Table 4 and Figure 6. Plantar mixed nerve latencies and responses were normal on the left, however, the responses were absent on the right. EMG of the only right foot intrinsic CASE REPORT OF A TRUE UNILATERAL TARSAL TUNNEL muscles (abductor hallucis and 4th dorsal interosseous) was ab- SYNDROME normal and had 1-2+ fibrillation potentials and positive sharp waves. A 35-year-old male who was seen for an EDX evaluation, had a few weeks history of pain, tingling, and numbness in the plantar

Figure 6 Normal left; but absent right plantar mixed nerve responses. 26 Tarsal Tunnel Syndrome AAEM Course

SUMMARY 8. Finkel JE. Tarsal tunnel syndrome: ankle & foot. Magn Reson Image Clin N Am 1994;2:67-78. 9. Galardi G, Amadio S Maderna L, Meraviglia MV, Brunati L, Dal Tarsal tunnel syndrome exists but is uncommon and sometime Conte G, Comi G. Electrophysiologic studies in tarsal tunnel overlooked. The most common problem is misdiagnosis or a syn.drome. Diagnostic reliability of motor distal latency, mixed nerve partially correct diagnosis. It often presents with vague symp- and sensory nerve conduction studies. Am J Phys Med Rehabil toms and signs may be difficult to elicit. The history often reveals 1994;73:193-198. prior trauma to the involved ankle. Tinel’s sign may be positive 10. Gatens PF, Saeed MA. Electromyographic findings in the intrinsic and hindfoot deformity may be present. A complete needle muscles of normal feet. Arch Phys Med Rehabil 1982;63:317-318. 11. Heimkes B, Posel P, Stotz S, Wolf K. The proximal and distal tarsal EMG/NCS assessment is required. The standard should include tunnel syndromes: an anatomical study. Int Orthop 1987;11:193- a bilateral study, and testing for medial and lateral plantar motor 196. and sensory conductions along with needle EMG study. 12. Irani KD, Grabois M, Harvey SC. Standardized technique for diag- Magnetic resonance imaging is helpful to identify space-occupy- nosis of tarsal tunnel syndrome. Am J Phys Med 1982;61:27-31. ing lesions. Once the diagnosis has been made, nonsurgical treat- 13. Johnson EW, Ortiz PR. Electrodiagnosis of tarsal tunnel syndrome. Arch Phys Med Rehabil 1966;47:776-780. ment may be indicated. Injections have limited success. If the 14. Kerr R., Frey C. MR imaging in tarsal tunnel syndrome. J Comp conservative non-operative treatment fails, then the surgical de- Assist Tomogr 1991;15:280-286. compression is the treatment of choice. The literature supports 15. Lau JC, Daniels TR. Tarsal tunnel syndrome: a review of the litera- up to 85-90% rate of improvement or resolution of symptoms ture. Foot Ankle Int 1999;20:201-209. with surgical release.23 However the specific cause of TTS must 16. Levin KH. Ischemic monomelic neuropathy. Muscle Nerve be addressed. 1989;12:791-795 17. Oh SJ. Clinical electromyography: nerve conduction studies, 2nd edition. Baltimore: Williams & Wilkins; 1993. 18. Oh SJ. Entrapment neuropathies of the posterior tibial nerve. REFERENCES Neurology Neurosurgery Update Series 1987;7:1-8. 19. Oh SJ, Kim HS, Ahmad BK. The near-nerve sensory nerve conduc- 1. Del Toro DR, Mazur A, Dwzierzynski WW, Park TA. tion in tarsal tunnel syndrome. J Neurol Neurosurg Psychiatry Electrophysiologic mapping and cadaveric dissection of the lateral 1985;48:999-1003. foot: implications for tibial motor nerve conduction studies. Arch 20. Oh SJ, Sarala P, Kuba T, Elmore R. Tarsal tunnel syndrome: electro- Phys Med Rehabil 1998;79:823-826. physiological study. Ann Neurol 1979;5:327-330. 2. DeLisa JA, Lee HJ, Barnan EM, Lai KS, Spielholz N, Mackenzie K. 21. Park TA, Del Toro DR. Electrodiagnostic evaluation of the foot. Phys Manual of nerve conduction velocity and clinical neurophysiology, Med Rehabil Clin N Am 1998;4:871-896. 3rd edition. New York: Raven Press; 1994. 22. Park TA, Del Toro DR. The medial calcaneal nerve: anatomy and 3. DeLisa JA, Saeed MA. Tarsal tunnel syndrome. Muscle Nerve nerve conduction technique. Muscle Nerve 1995;18:32-38. 1983;6:664-670. 23. Reade B, Longo D, Keller M. Tarsal tunnel syndrome: chronic ankle 4. Dumitru D. Electrodiagnostic medicine. Philadelphia: Hanley and pain. Clin Podiatr Med Surg 2001;18:395-408. Belfus; 1995. p 905-908. 24. Saeed MA, Gatens PF. Compound nerve action potentials of the 5. Eisele AS. Conditions of the toenails. Orthop Clin North Am medial and lateral plantar nerves through the tarsal tunnel. Arch Phys 1994;1:183-188. Med Rehabil 1982;68:304-307. 6. Erickson SJ, Quinn SF, Kneeland JB, Smith JW, Johnson JE, Carrera 25. Saeed MA, Oh SJ, Singh S, Falco F. Entrapment neuropathies in the GF, Shereff MJ, Hyde JS, Jesmanowicz A. MR imaging of the tarsal lower extremity. Rochester, MN: American Association of tunnel and related spaces: normal and abnormal findings with Electrodiagnostic Medicine; 2001. anatomic correlation. AJR Am J Roentgenol 1990;55:323-328. 26. Schon LC. Nerve entrapment, neuropathy, and nerve dysfunction in 7. Felsenthal G, Butler DH, Shear MS. Across-tarsal-tunnel motor athletes. Orthop Clin North Am 1994;25:47-59. nerve conduction technique. Arch Phys Med Rehabil 1992;73:64- 27. Steinitz ES, Singh S, Saeed MA. Diagnostic tests help clarify tarsal 69. tunnel mystery. BioMechanics 1999;6:43-51. 27

Nonneurogenic Causes of Foot Pain

Atul T. Patel, MD, MHSA Kansas City Bone and Joint Clinic Kansas City, Missouri

INTRODUCTION EVALUATION

Physicians are seeing more patients with foot and ankle prob- History lems. There were greater than 14.2 million visits to physician’s offices in 2001 because of foot or ankle problems. Ankle sprains In addition to checking a patient’s general history, the physician and fractures account for 2.3 million and 1.2 million visits re- must check for a history of trauma preceding the onset of pain. spectively.1 A great amount of stress and pressure is placed on this A history of trauma is usually the most likely cause of pain. The area of the body. Walking one mile generates more than 60 tons quality of pain in the foot, as in other parts of the body, needs to of stress on each foot. Feet cushion up to one million pounds of be assessed. Moreover, it is important to ask questions about the pressure during one hour of strenuous exercise. Hence, it is not timing of the pain. Is the pain worse in the morning? Also, what surprising that more than 20% of musculoskeletal problems makes the pain worse? At what part of the gait cycle is the pain affect the foot and ankle.9 worst (particularly heel rise), or is the pain worse with just weight bearing? Other issues include other underlying systemic diseases Electrodiagnostic (EDX) consultants are often faced with evalu- such as gout, diabetes mellitus, or rheumatoid arthritis. Is there ating patients with foot and ankle pain. Not all such pain is as- a history of previous surgery? If so, is there any change in the sociated with neuropathic causes. Oftentimes, patients with pain compared to pre- and post-surgery and the present time? acute pain of the foot and ankle present to their primary care physician, such as a family practitioner or internal medicine Examination physician. At other times, they are seen by an orthopedic surgeon, but once the pain becomes chronic, they are more likely The examination begins with inspection as the patient enters the to be referred to other specialists, including neurologists and examination room. First, the physician needs to inspect the ex- physiatrists for further assessment. Electrodiagnostic consultants ternal appearance of the shoe since the shoe can give several clues need to understand the causes of foot pain, especially chronic to the patient’s foot deformity. For example, the shoes of an in- foot pain. This manuscript will focus on musculoskeletal abnor- dividual with flat feet usually have broken medial counters due malities of the ankle and foot, with specific attention being paid to the prominence of the talar head. Scuffing of the front of the to functional anatomy and regional localization of the common shoe may be due to a foot drop. The absence of creases over the pain syndromes. dorsal aspect of the shoe may indicate a lack of toe off. Next, the 28 Nonneurogenic Causes of Foot Pain AAEM Course physician should assess the patitent’s foot. When inspecting the the foot examination, further assessment of the rest of the body foot, assess for alignment of the great and lesser toes, the position may be warranted. of the foot in relation to the limb and medial curvature of the forefoot. Inspect the arch and undue prominence of the medial midfoot. Also during inspection, compare one foot with the ANATOMY other to assess for asymmetry. Assess for callosities, swelling, or skin breakdown. Check for overlapping toes or bunion defor- The ankle and foot can be divided functionally into four sec- mity. The examining physician must also view the alignment of tions: the ankle, the hindfoot, the midfoot, and the forefoot. the heel posteriorly. Normal posture is neutral or slight valgus Problems in these areas can be further assessed on physical ex- (turned out heel), with no more than one or two lateral toes amination based on the patient’s symptoms. visible from behind. When the patient stands on the toes, the heel should move into normal varus position. It is also important Ankle to assess the patient’s gait and deviations from a normal gait pattern. Analyze the alignment of the foot during the different The ankle is the junction of the distal lower extremity and the phases of gait, including heel strike, mid-stance, toe off, and foot. It is a hinged joint formed by the tibia, fibula, and talus. swing phase.8 The tibia and fibula provide medial and lateral stabilization (mortise, malleoli). This configuration is maintained by three The next portion of the examination consists of palpation of the sets of ligaments: the deltoid ligament, the lateral collateral liga- soft and bony structures of the foot and ankle. Over the medial ment, and the syndesmosis. It is estimated that more than aspect of the foot, palpate the medial malleolus or just inferior to 27,000 individuals sprain an ankle each day in the United States. this location. In patients with posterior tibialis dysfunction, there The hallmarks of this condition are ankle swelling, pain, and may be swelling and tenderness along the course of the posterior often ecchymosis. Chronic ankle pain usually occurs at the an- tibial tendon. Palpate both sides of the Achilles’ tendon inser- terolateral aspect of the ankle. Problems include instability, tion. Findings of swelling or tenderness are signs of retrocal- injury to peroneal tendons, occult fracture, and subtalar synovi- caneal bursitis. Laterally palpate behind and below the fibular tis. malleolus to identify tenderness or swelling associated with peroneal tenosynovitis or subluxation of the tendons with active Hindfoot dorsiflexion and plantar flexion of the ankle. In addition to examining the patient for tenderness and swelling, it is important Plantar fasciitis is the most common problem in the hindfoot. to assess for range of motion (ROM) of the ankle with dorsi- Other problems include posterior tibial dysfunction leading to a flexion and plantar flexion, inversion and eversion, supination flat foot. The proximal and posterior division of the hindfoot is and pronation. Muscle testing is also a necessary part of the ex- formed from the articulation of the talus and calcaneus and the amination. In addition to the routine tests of strength in the midfoot junction with the medial navicular and the lateral lower extremity, muscle testing, should include testing of the cuboid bones. The motion of the hindfoot is subtalar motion posterior tibialis, anterior tibialis, peroneus longus and brevis, from the movement between the talus and the calcaneus, and extensor hallucis longus, and flexor hallucis longus muscles.6 the talar, navicular, and calcaneal articulation. Isolating the true hindfoot from midfoot movement is accomplished by grasping Certain special tests can also be carried out, including (1) the an- and steadying each area in turn and repeating the ROM. terior drawer test to test stability of the anterior talofibular liga- Functionally, the hindfoot serves the foot by dissipating the ment, (2) the varus stress test can be used to assess for laxity of impact forces of heel strike and sitting as mediator between the calcaneal fibular ligament, (3) the metatarsophalangeal joint in- motion of the lower extremity and the rest of the foot. Pain from stability test to assess for instability which is often present after the hindfoot is described by patients as heel pain, but has many chronic synovitis or long-standing claw toe deformity. In addi- proximal or distal origins. The hindfoot can be further function, a physician should palpate the metatarsal bones and inter- tionally broken down into the posterior, inferior, medial, and digital spaces. Tenderness in the interdigital space while lateral hindfoot. The posterior hindfoot includes the Achilles’ squeezing the forefoot could represent a neuroma. tendon and the calcaneus, and internally between these two structures lies the retrocalcaneal bursa. The inferior hindfoot In general, when assessing a patient with an ankle or foot structures include the area between the calcaneus and the plantar problem, comprehensive inspection of the lower back and lower surface of the foot. These are the subcalcaneal fat pads underly- extremity should be carried out. Depending on the findings of ing the skin, branches of the posterior tibial nerve, and the AAEM Course Painful Foot and Ankle 29 plantar fascia with its proximal attachment to the medial calca- coexist and their symptoms can overlap, which further compli- neus. The medial hindfoot consists of the broad medial collateral cates assessment and diagnosis. (deltoid) ligament. Below this is the spring ligament, which stretches between the navicular and the calcaneus to support the Plantar Fasciitis. The most common cause of plantar heel pain talus. Posterior to the medial malleolus lie the tibialis posterior is proximal plantar fasciitis (PPF). This was called heel pain syn- tendon and the neurovascular bundle. The lateral hindfoot con- drome by Wood in 1812. Since then, several different names sists of the lateral collateral ligament.9,10 have been used in the literature, all essentially describing the same syndrome. Plantar fasciitis is reportedly the most common Midfoot cause of pain in the inferior heel and it is estimated to account for 11-15% of all foot symptoms requiring professional care Chronic dorsal midfoot pain is commonly due to degenerative among adults. Reliable population-based incidence data are arthritis involving the midfoot joints. Pain in the plantar aspect lacking, although plantar fasciitis has been reported more com- of the midfoot is unusual. The midfoot consists of two rows of monly in runners and those who are military personnel. The in- bones sandwiched between the two hindfoot bones and the five cidence peaks between the ages of 40 and 60 in the general metatarsals. Two bones make up the proximal row: the medial population. The distribution of men to women affected varies navicular and the lateral cuboid. The distal row consists of three from study to study and the condition can be present bilaterally small cuneiform bones. Most midfoot motion is limited to the in up to one-third of the cases. The risk factors for plantar fasci- talus, navicular, and calcaneus. The midfoot has several dynamic itis are poorly understood and are probably multifactorial. Based structures, including the longitudinal arches and the horizontal on limited case control type of studies, the most common cited arches.6,9 risk factors include obesity, prolonged standing, long distance running, and heel spurs (inferior calcaneal exostoses). Patients Forefoot typically complain of a nonradiating pain localized to the medial plantar surface of the calcaneal tuberosity. It is most severe on The forefoot consists of the metatarsals and phalanges. The distal arising in the morning and taking the first few steps. During the metatarsal heads are held in place by ligaments and muscles of night, the foot is in an equinous position and the fascial tissues the forefoot. Forefoot problems occur nine times more fre- contract. With weight bearing in the morning or after a pro- quently in women, and this is attributed to their footwear. Other longed period of rest, the fascia is instantly placed under tension, causes of forefoot pain include bunions, hammer toes, claw toes, aggravating the inflammation. It is also painful after long rests or ingrown toenails, metatarsalgia, and interdigital neuromas. If the at the end of a day of prolonged walking or standing. Patients examining physician finds tenderness in the distal metatarsals, it can often localize a spot on the heel that is the center of the ten- should raise the suspicion of a stress fracture.5,9 derness. With the prolonged symptoms, patients may develop an antalgic gait and begin toe walking or walking with weight bearing on the lateral side of the foot in order to avoid placing ANKLE AND FOOT PAIN SYNDROMES weight on the heel. Paresthesias are uncommon.

Inferior Hindfoot The etiology of PPF is somewhat obscure. Histologic examination of specimens from patients who have undergone plantar Pain in the hindfoot is often described as heel pain by patients. fascial release show degenerative changes in the plantar fascia There are several causes of pain with origins distal and proximal with all of the fibroplastic proliferation and chronic inflamma- to the heel. Pain in the heel is common and can often be frus- tory changes. It is thought that micro-ruptures and hemorrhage trating both for the patient and the physician. The pain can be in collagen degeneration may develop in the fibers leading to fi- dispensed in two anatomic areas, the inferomedial heel and the brosis and ossification of the muscular and fascial layers as well posterior superior heel. There is confusion in the diagnosing and as periostitis of the calcaneus. The theory that heel spurs directly treatment of heel pain, partly due to the complexity of the local cause the pain is no longer accepted. Only 50% of patients with anatomy. Causes of heel pain include seronegative arthritides, heel pain have calcaneal spurs. Conversely, 15% of patients that heel spur, fracture, calcaneal stress fracture, plantar fasciitis, bur- do not have heel pain have calcaneal spurs. sitis, complete or partial plantar fascial rupture, lumbosacral radiculopathy, and entrapment of the nerve to the abductor Some patients may have pain more distally in the plantar fascia. digiti quinti muscle (Baxter’s nerve). Several conditions may This is referred to as distal plantar fasciitis and may have similar 30 Nonneurogenic Causes of Foot Pain AAEM Course epidemiology as PPF. The onset may be gradual or acute when often leads to the development of a prominence of the postero- caused by trauma. It is also believed that distal plantar fasciitis is superior part of the calcaneus (Haglund’s deformity). Patients a degenerative inflammatory process that may be initiated by complain of gradual or acute onset of pain at the level of the in- repetitive stress or minor trauma. The pain is usually most pro- sertion of the tendon. Pain and inflammation are increased with nounced in the mid arch. Plantar fascial rupture may be seen activity.8 after multiple injections of cortisone. The patient may note swelling and tenderness following a painful snap, pop, or tearing Retrocalcaneal Bursitis. Retrocalcaneal bursitis is an inflamma- sensation.4,7 tion of the retrocalcaneal bursa, which is lined with synovial cells. It is a disorder that occurs in all ages and occurs in both Heel Pad Atrophy. Heel pad atrophy is a chronic condition that males and females. It is caused by overuse and repetitive trauma, is associated with aging as the construct of the fat pad breaks impingement of the calcaneus, or increased range of dorsiflex- down. Patients are typically middle aged and older. Bilateral in- ion. Retrocalcaneal bursitis often occurs in conjunction with involvement of the heel pads is uncommon, but does occur. sertional tendinitis and is a component of Haglund’s syndrome. Patients usually complain of gradual onset of pain that is nonra- Patients complain of pain at rest that increases with activity. diating with maximal tenderness in the central heel occasionally expanding to the heel perimeter. Pain is most severe after pro- Adventitial Bursitis. Adventitial bursitis is the soft tissue re- longed walking, especially in uncushioned hard-soled shoes on sponse that develops over the proximal posterolateral aspect of nonresilient surfaces. The pain is not as severe in the morning. the calcaneus. This is a combined bone and soft tissue entity seen most commonly in females who wear pump-style shoes and Other causes of heel pain include tumor, infection, and stress therefore is known as a “pump bump.” Shoe wear is responsible fracture. A stress fracture can occur in both the calcaneus and in for creating an adventitial bursitis because the shoe is held onto the spur itself. If a stress fracture is present, squeezing the body the foot by a stiff heel counter contoured inward at the tip to of the calcaneus produces medial and lateral pain. Finally, they prevent the back of the shoe from falling off the foot. The pos- examining physician must consider seronegative spondy- terolateral bone ridge can hypertrophy in response to this irrita- loarthropathies, especially when the pain in the heel is bilateral. tion. The bursa becomes endocytic and inflamed, making it Often these patients have enthesopathies (pain at the insertion of difficult for the skin to glide smoothly over the bone. This soft tendons and ligaments into bone). The pain is variable and shift- tissue inflammation is the predominant finding of a pump ing in nature and often multiple joints are involved. bump. The patient usually complains of pain with pressure on the posterior heel, as well as a palpable bump that slowly enlarges Posterior Hindfoot causing pain with shoe wear.

Posterior heel pain is a less common entity. The pain in this area Haglund’s Syndrome. Haglund’s syndrome is a combination of is usually associated with activity rather than weight bearing. insertional tendinitis, retrocalcaneal bursitis, adventitial bursitis, Again, it is confusing to diagnose individual conditions given the and an enlarged bursal prominence. The presence of an isolated type of presentation and overlap in symptoms. pump bump does not implicate Haglund’s syndrome. The syndrome is characterized by a painful soft tissue swelling at the level Achilles’ Tendinitis. The Achilles’ tendon is the strongest of the insertion of the Achilles’ tendon, a defined calcaneal tendon in the body. It is covered by a paratenon instead of a def- prominence on lateral radiograph, and a visible and palpable soft inite tendon sheath. The tendon is hypovascular about 2-6 cm tissue swelling. The patients can be of all ages, although they are proximal to the osseous insertion. The disorders of the Achilles’ predominantly female. tendon are classified as either insertional or non-insertional. Noninsertional tendinitis usually occurs in the hypovascular Medial Hindfoot region, usually due to overuse or overtraining. Insertional tendinitis is a condition of pain at the insertion of the Achilles’ Posterior Tibial Tendon Dysfunction. Medial ankle pain is tendon with or without calcification. It is more common in commonly due to disorders of the posterior tibial tendon. This young adults. It is thought that the tendon undergoes fibrovas- tendon inserts into the tuberosityof the navicular bone with slips cular degeneration and reparative fibrosis within and around the to the cuneiforms, cuboid, and bases of the second, third, and tendon causing thickening in the posterior heel. The condition fourth metatarsals. It serves to balance the pull of the peroneal is best described as a combination of degeneration of the tendon tendons, protects the spring ligament, and inverts and stabilizes and cystic changes in the posterior calcaneal tuberosity. This the hindfoot during toe-off. Dysfunction of this tendon can AAEM Course Painful Foot and Ankle 31 occur from inflammation, degeneration in hypovascular areas, of the sole. Symptoms are exacerbated by weight bearing and trauma, and steroid injections. Problems lead to the develop- dorsiflexion, and relieved with rest and plantar flexion. Typical ment of a flat foot. patients are overweight and deconditioned, or may be athletes who place inappropriate demands on a well-conditioned foot, or Lateral Hindfoot normal individuals who exceeds the normal weight-bearing activity. Ankle Sprain. The most common cause of pain in the lateral ankle area is an ankle sprain. More than 27,000 individuals Plantar sprain an ankle each day in the United States. Acute anterolateral ankle pain, swelling, and frequently ecchymosis are the hall- Plantar Fibromas. Plantar fibromas can present problems in the marks of this condition. Ankle sprain is also the most common feet associated with weight bearing. They are similar to of all sports-related injuries. In 95% of ankle sprains, the lateral Dupuytren’s contracture of the palmar aponeurosis. Other collateral ligament is affected through excessive foot inversion causes of plantar midfoot pain include puncture wounds and with soft tissue and ligamentous stretch. There is often associated trauma, plantar fasciitis, and tendonitis.2 micro-hemorrhage and edema. Of the three ligaments that com- prise the lateral collateral ligament, the most frequently injured Dorsal Midfoot is the anterior talofibular ligament (ATFL). Isolated sprain here causes instability of the anterior motion. The calcaneal fibular Dorsal midfoot pain is often related to improper or tightly-laced ligament is involved in 15-25% of lateral injuries, but almost shoes. This can result in extensor tendonitis and can be exacer- always with the ATFL. The posterior talofibular ligament sprain bated by bony spurs (exostoses). The pain is usually diffuse and is uncommon and usually means the entire complex is injured. accompanied by erythema. Continued stress on tendon sheaths Ankle sprains are graded according to the extent of injury and can lead to the formation of ganglion cysts. Another cause of instability. Several classification systems for grading lateral ankle dorsal midfoot pain is degenerative joint disease. This can be a sprains exist. The most common system is based on the clinical consequence of an old fracture, trauma, or avascular necrosis of examination. In this system, Grade I ankle sprains are painful, the talar and navicular bones. The patient usually presents with but have a full ROM. There is no pain during weight bearing. dorsomedial pain and swelling. Pain is worse with weight There is no increased laxity when compared to the uninjured bearing and tarsal squeeze. Pain also can be associated with en- side. This correlates with mild stretching of the ATFL. Grade II trapment of the deep peroneal nerve (anterior tarsal tunnel syn- ankle sprains are painful with increased laxity on testing. There drome). may be associated swelling and decreased ROM, difficulty with pain during weight bearing and ambulation. This corresponds Forefoot with a partial tear of the calcaneal fibular ligament and a complete tear of the ATFL. Grade III ankle sprains are usually Metatarsal Fractures. The metatarsal site of the foot accounts painful with an unstable ankle joint and correlate with a com- for the greatest percentage of fractures in the foot. Fractures of plete rupture of both the ATFL and calcaneal fibular ligament.4 the metatarsals generally result from direct trauma, often from a heavy object dropped onto the dorsum of the foot. Stress frac- Anterior Hindfoot and Ankle tures can develop in the metatarsals, especially with a sudden increase in activity, such as running longer distances. Consider a Osteochondral Lesions of the Talus. A common diagnosis in stress fracture when a patient presents with recent onset of pain patients presenting with chronic ankle pain is delayed diagnosis over the metatarsals, especially in the distal aspects of the second of osteochondral lesions of the talar dome. Patients usually have or third metatarsals.9 symptoms of ankle pain, recurrent swelling, ankle instability, or the feeling of locking of the ankle. Lesions in the anterior talus Hallux Rigidus and Hallux Valgus. Degenerative arthritis can are thought to be caused by trauma, such as an inversion ankle develop in any of the joints of the forefoot, but occurs most injury. Medial lesions are suspected to be associated with degen- commonly in the first metatarsophalangeal joint. This results in erative cysts. the development of hallux rigidus. This can be painful with attempted dorsiflexion of the hallux and can result in altered Medial Midfoot weight bearing. Rheumatoid arthritis affects the forefoot and the most common changes seen involve hallux valgus deformity. Medial Longitudinal Arch Strain. Pain in the midfoot is Hallux valgus deformity can also result from pes planus (flat usually due to strain of the medial longitudinal arch. This arch foot) or a long first metatarsal. provides the spring for foot propulsion. Fatigue and strain result from acute or chronic stress and overuse. Patients usually have Biomechanical Imbalance. Pain-free motion requires both aching pain that is reproducible along the medial plantar border normal forefoot alignment and maintenance of the arches. 32 Nonneurogenic Causes of Foot Pain AAEM Course

Disruption in this framework creates a pathologic cycle of bone osteosarcomas occur in adolescents and young adults, and malalignment, muscle imbalance, and altered biomechanics that myelomas and metastatic diseases occur in older adults.7 The may result in forefoot pain. The most common culprit in the de- most malignant tumor of the foot is melanoma. Although velopment of forefoot problems is tight fitting shoes.4,9 Friction melanoma accounts for approximately 1-3% of all cancers, 6% from within the shoe results in corns on top of the toes, plantar of melanomas occur in the foot. calluses, ingrown toenails, and bunions. Systemic Disorders Hammer Toes. Hammer toe is a “buckling” of a toe with extension at the metatarsophalangeal joint and flexion at the prox- Systemic conditions such as rheumatoid arthritis, gout, pseudo- imal interphalangeal joint. This deformity is characterized by a gout, diabetes, and other arthritic conditions can also cause contracture of the flexor digitorum longus tendon which is due changes in the feet with associated pain. Other conditions to to poor-fitting shoes or an underlying neuromuscular disorder. consider are peripheral vascular disease, infections, and peripheral neuropathy. Claw Toes. The etiology of claw toes is unclear. The deformity is characterized by contractures of the long flexors and extensors of the toe. This results in distal and proximal interphalangeal SUMMARY joint flexion and hyperextension of the metatarsophalangeal joint. Foot and ankle pain is a common problem and accounts for up to one fifth of all musculoskeletal problems. Electrodiagnostic Metatarsalgia. Metatarsalgia is a generic term indicating pain lo- consultants need to be aware of the major causes of non-neuro- calized in the ball of the foot. The pain is usually located over the pathic causes of foot pain to better manage patients with foot metarsal heads and is related to activity. Metatarsalgia is due to pain. The key to appropriate diagnosis is an appropriate medical static imbalance in the weight distribution across the metatar- history and examination to determine the exact location of the sophalangeal joint resulting in increased pressure under each pain and duration of the symtoms. Most common pain syn- joint. dromes of the foot and ankle involve the hind foot.

OTHER CAUSES OF FOOT PAIN References

Tumors 1. American Academy of Orthopaedic Surgeons. The foot and ankle. Available at: http://orthoinfo.aaos.org/fact/thr_report.cfm? thread_id=100&topcategory=Foot;. Accessed July 15, 2004. Benign neoplasms and malignancy in the foot can be a cause of 2. Brinker MR, Miller MD. Fundamentals of orthopaedics. pain. Primary musculoskeletal malignancies are rare compared Philadelphia: WB Saunders; 1999. p 342-363. to benign tumors. Based on the literature reviewed, it is difficult 3. Buchbinder R. Clinical practice. Plantar fasciitis. N Engl J Med to comment on the incidence of benign neoplasms in the foot, 2004;350:2159-2166. given the fact that many are asymptomatic and discovered inci- 4. DiGiovanni BF, Partal G, Baumhauer JF. Acute ankle injury and dentally. Of the 5000 primary musculoskeletal sarcomas diag- chronic lateral instability in the athlete. Clin Sports Med 2004;23:1- 20. nosed yearly in the United States, fewer than 5% arise in the 5. Hockenbury RT. Forefoot problems in athletes. Med Sci Sports Exerc foot. Although these tumors are rare, they can present as pain in 1999;31:S448-S458. the foot and ankle area. Primary musculoskeletal neoplasms 6. Hoppenfeld S. Physical examination of the spine and extremities. grow and expand within discrete, compact compartments. There New York: Appleton-Century-Crofts; 1976. are four plantar and two dorsal soft tissue compartments in the 7. Jaffe KA, Jones FK. Foot tumors. In: Gould JS, Thompson FM, Cracchiolo A, editors. Operative foot surgery. Philadelphia: WB foot. Compared to other areas in the body, these are not as dis- Saunders; 1994. p 240-262 tinct and are not effective barriers to tumor extension. 8. Mizel MS, Hecht PJ, Marymont JV, Temple HT. Evaluation and Consequently, soft tissue extension of primary bone lesions treatment of chronic ankle pain. J Bone Joint Surg Am 2004;86:622- occurs in the foot, especially with locally aggressive and malig- 632. nant tumors. Despite high functional demands and condensed 9. Pfeffer GB, Balderson RA, Baumhauer JF. Foot and ankle pain. In: anatomy, early symptoms of soft tissue sarcoma are the exception Greene W, Snider K, editors. Essentials of musculoskeletal care, 2nd edition. Rosemont, IL: American Academy of Orthopaedic Surgeons; and not the rule. Patients with foot tumors may present with 2001. pain and impaired function, with or without a palpable mass. 10. Sarrafian SK. Anatomy of the foot and ankle: descriptive, topo- The age of the patient can help differentiate some of the tumors. graphic, functional, 2nd edition. Philadelphia: Lippincott Williams For example, Ewing’s sarcomas occur in preadolescents, & Wilkins; 1993. 33 Surgical Management of Entrapment Neuropathies in the Foot, Including Indications and Outcomes

Mark E. Easley, MD Assistant Professor Division of Orthopaedic Surgery Duke University Medical Center Durham, North Carolina

Lew C. Schon, MD Department of Orthopaedic Surgery The Union Memorial Hospital Baltimore, Maryland

INTRODUCTION effect may manifest itself clinically. A typical example is a herni- ated disc creating proximal nerve root impingement and resul- Nerve dysfunction of the foot and ankle is frequently under- tant impairment of axoplasmic flow, exacerbating an otherwise diagnosed because such problems are often poorly localized, asymptomatic mild tibial nerve (TN) compression in the tarsal masked by other injuries, or dynamic in nature. The most im- tunnel. The double-crush syndrome does not necessarily have to portant element in the evaluation of the patient with pain in the involve two distinct areas of nerve compromise; instead, two dif- leg, ankle, or foot is an awareness of these syndromes. The physi- ferent mechanisms of nerve compromise may be responsible for cian should be familiar with the common clinical characteristics the phenomenon. Diabetes mellitus or alcoholism may make a of nerve disorders and possess a sound understanding of the neu- nerve more susceptible to peripheral compression.29,81 roanatomy of the foot and ankle. The aim of this manuscript is to review the major nerve syndromes of the foot and ankle, in- An important factor in the evaluation of nerve disorder of the cluding discussions of etiology, evaluation, and management. lower extremity is that the syndrome may be static or dynamic. A static nerve disorder is present at rest, whereas a dynamic nerve disorder presents only with activity. Frequently, a static examina- OVERVIEW/TERMINOLOGY tion of a dynamic nerve syndrome fails to reveal the patient’s symptoms, whereas an evaluation after exercise or activity which Because of the diffuse nature and often poor localization of nerve produces the symptoms may uncover findings leading to proper pain, evaluation of distal lower extremity nerve symptoms must diagnosis. When assessing a patient with neuralgia or nerve pain, include an assessment of systemic disease, metabolic disorders, it is useful to categorize the neuralgia as nociceptive or ectopic. chemical exposure, medications, alcohol abuse, and other central Nociceptive neuralgia is nerve pain that is induced by mechani- or peripheral neurologic syndromes that may be responsible for cal stimulation, such as touching or twisting. Ectopic neuralgia any pain in the foot and ankle. The double-crush phenomenon is nerve pain that is spontaneous and unprovoked. Although may also be responsible for extremity nerve pain and must be as- ectopic neuralgia may be increased with certain mechanical sessed.18,89,103,104,113 In a double-crush situation, a nerve is affected stresses, clinical manifestation does not depend on these triggers. in two separate locations. Each focus of nerve compromise taken Nerves with ectopic symptoms usually have more internal or in- in isolation may remain subclinical; however, the cumulative trinsic nerve damage than those with nociceptive symptoms. 34 Surgical Management of Entrapment Neuropathies in the Foot, Including Indications and Outcomes AAEM Course

Etiologic considerations apply to all nerves and warrant defini- the branching pattern. Bifurcation of the TN into its two main tion. A nerve may be injured by stretch, contusion, or transec- branches, the MPN and the LPN, is typically assessed in refer- tion. A stretch or contusion may occur as a one-time event or ence to the tarsal tunnel, coursing under the flexor retinaculum may happen repetitively. In an overuse nerve syndrome repetitive that spans between the medial malleolus and calcaneus. stretching or contusion may occur numerous times in a subclin- Bifurcation in the tarsal canal occurred in 69-96% and proximal ical fashion before manifesting. In more acute traumas, the to the tarsal canal in 4-31% of specimens. The MCN frequently stretch or contusion may present with nerve symptoms immedi- comprises multiple branches, with studies suggesting more than ately or, occasionally, in a delayed fashion. one medial calcaneal branch in up to 60% of specimens. These branches may originate both within, proximal to, and distal to Entrapment syndromes occur either from these overuse mecha- the tarsal canal, and have been shown to stem from the TN, nisms or it may follow a more acute trauma. In an entrapment MPN, or LPN, although the majority of specimens have syndrome, a band of tissue external to the nerve (i.e., fascia, demonstrated that the MCN is a branch of the TN. The MPN muscle, bone, or scar tissue) impinges on the nerve. When the further divides into plantar branches that innervate intrinsic scar tissue engulfs the nerve (usually after open trauma, surgery, muscles of the foot and provide plantar sensation. The LPN has or infection), the condition may be referred to as adhesive neu- similar but more lateral divisions, after giving off its first branch ralgia. Clinical hallmarks of adhesive neuralgia are decreased (FBLPN), which courses anterior to the medial calcaneal range of motion of the adjacent joint and a tender, thickened, or tuberosity and innervates the abductor digiti minimi and occa- immobile scar. sionally the flexor brevis. The relative orientation of the various branches varies. In general, the MCN and the FBLPN lie medial Transection injury may be partial or complete, and it may result to the MPN and LPN. The MPN lies anterior to the LPN. in a complete neuroma or in a neuroma in continuity. After any More proximal to the tarsal tunnel, anatomic intercommunica- injury, the territory of the affected nerve can exhibit a variety of tions increase in number and the fascicular bundles become less symptoms: paresthesia (tingling, electric sensations that are not distinct. necessarily painful), dyesthesia (painful nerve symptoms), hy- pesthesias (decreased sensitivity), hyperesthesia (increased sensi- Tarsal Tunnel Syndrome tivity), allodynia (nonpainful stimuli resulting in pain perception), or anesthesia (numbness). Loss of afferent nerve Overview conduction usually results in a deafferentation phenomenon, which produces more anesthesia in the zone of the damaged af- Although the first description of TN entrapment in the tarsal ferent nerve and hyperesthesia or dyesthesia in the surrounding canal dates back to 1960, it was not until 2 years later that the territory. Often, nontraumatized adjacent nerves will be sensitive term tarsal tunnel syndrome (TTS) was introduced. The syn- to palpation because these adjacent nerves carry pain signals drome is defined as compression or compromise of the TN or its from the damaged territory. The term anesthesia dolorosa refers branches under the posteromedial flexor retinaculum of the to a zone of numbness that is painful to touch. ankle and foot. Some authors refer to compromise of any of the TN components as TTS, whereas others distinguish between The five major nerves innervating the foot and ankle are the proximal compression of the TN trunk and more distal com- tibial, saphenous, superficial and deep peroneal, and sural pression of terminal nerve branches. To best define clinical enti- nerves. Although compromise may occur at any location along ties and anatomic correlations, syndromes affecting individual the course of a peripheral nerve or its branches (see individual nerve branches will be presented independently in this discus- nerve sections below), typical foci are recognized and generally sion. related to specific anatomic structures (see individual nerve sections below for characteristic syndromes). Etiology

Tarsal tunnel syndrome, or compromise of the TN, may be id- TIBIAL NERVE AND BRANCHES iopathic2,31,61,76 but reviews of the literature suggest that a specific cause can be identified in up to 82% of patients.19,75,122 Anatomy Approximately 33% of the identifiable causes are related to trauma or post-traumatic arthritis, including gan- The TN is a component of the sciatic nerve, coursing along the glions,64,75,79,121,122 exostoses/fracture fragments, scar tissue/fibro- posteromedial aspect of the ankle, where it divides into the sis, compartment syndrome after calcaneus fractures,86 and medial plantar nerve (MPN), lateral plantar nerve (LPN), and valgus hindfoot malalignment producing stretch of the TN.76 medial calcaneal nerve (MCN) branches. Although the TN con- Other space-occupying lesions include varicosities,35,43 inflam- sistently separates into these three main divisions, cadaveric mation related to rheumatologic conditions, tumors 55,87,121 and studies have demonstrated a considerable amount of variation in anomalous musculature.31,105 The development of tarsal tunnel AAEM Course Painful Foot and Ankle 35 symptoms has also been related to bony prominences of talocal- authors have had patients jog, exercise, or dance before or during caneal coalitions.122 As noted above, the etiology may be sec- the appointment to expose the symptomatology. Finally, a com- ondary to pathology observed only in dynamic situations.76 prehensive evaluation should include tests to rule out radiculopathy (i.e., straight leg raises) or to look for more generalized Anatomy findings.

The tarsal canal is a fibroosseous tunnel enclosed by the flexor Diagnostic tests. Radiographs may be helpful in identifying retinaculum stretching from the posterior aspect of the medial bony deformity, including joint malalignment, coalition, exos- malleolus to the posterior process of the talus and calcaneus. The toses, loose bodies/fragments, or even foreign bodies. Further flexor retinaculum is attached to the sheaths of the posterior bony deformity or soft-tissue pathology may be defined with the tibial, flexor digitorum, and flexor hallucis longus tendons. The use of computed tomography scanning, but magnetic resonance TN courses within this fibroosseous tunnel with the posterior imaging (MRI) is better in the evaluation of suspected soft-tissue tibial artery and one of two veins. As noted above, the TN ter- masses or pathology in the tarsal canal. Laboratory studies may minal branches frequently within the tarsal canal, but with a be beneficial in diagnosing systemic causes for TTS and are in- variable pattern. dicated, but may be unreliable.

Evaluation Electrodiagnostic (EDX) studies, including sensory and motor nerve conduction studies (NCSs) and needle electromyography History. The patient with TTS may have difficulty localizing (EMG), can be helpful in the assessment of TTS. Evidence of symptoms, but usually describes medial or posteromedial foot entrapment (such as prolonged distal latency and decreased am- and ankle pain. The area of pain usually extends along the course plitude) and evidence of axonal damage (such as denervation and distribution of the nerve. Typical symptoms include of radi- findings) on needle EMG can be helpful for prognosis and treat- ation of pain to the plantar aspect of the foot, and occasionally, ment. Although some clinicians suggest that EDX studies are ap- radiation of pain proximally along the medial aspect of the calf. proximately 90% accurate in confirming TTS, other The pain, usually characterized as burning, electric, shooting, investigators have noted that these studies fail to correlate with stabbing, tingling, or numbing, is generally exacerbated by ac- surgical findings or postsurgical outcome.59,91 In a comprehen- tivity and relieved by rest. It is possible that symptoms may be sive review of the literature pertaining to TTS, Cimino19 con- present at rest, possibly related to compression created by pos- cluded that, overall, EDX studies are specific, yet insensitive. The tural pressure during sleep. The type of activity and specific current authors find that EDX studies should assess not only the movements or positions that exacerbate the pain should be iden- affected nerve, but all of the peripheral nerves in that lower ex- tified. Finally, any history of systemic disorders that may affect tremity and in the contralateral extremity as well. A complete nerves must be noted. In addition, trauma, medications, chem- EDX study allows for identification of localized nerve involve- ical exposure, alcohol abuse, or low back pain with radiculopa- ment as well as findings suggestive of radiculopathy or peripheral thy should be documented. neuropathy.59

Physical examination. The patient should be examined in the Management weightbearing position to assess overall alignment of the foot and ankle, especially to assess for valgus hindfoot malalignment Nonoperative. Nonoperative measures may prove to be effective that may stretch the TN. Claw toe deformities or intrinsic in the treatment of patients with TTS, but are rarely successful wasting may be indicative of advanced TN dysfunction. Any re- if space-occupying lesions are responsible for the symptomatol- striction to range of motion of the ankle and hindfoot may be ogy.19 If inflammation is contributing to nerve compromise, indicative of previous injury or degenerative change. Synovitis, nonsteroidal antiinflammatory agents (NSAIDs) may alleviate edema, tendinitis, or venous insufficiency may produce symp- symptoms.19 Occasionally, corticosteroid injections can improve toms from TN irritation. Palpation of the posterior and medial inflammation, especially if the focus of entrapment can be local- aspect of the ankle may identify mass effects of soft-tissues or ized. In most cases, however, relief of symptoms is only tran- even bony prominences or loose bodies. Percussion along the siently.19,76 Symptoms in the tarsal tunnel may also result from course of the TN may produce paresthesias or dyesthesias in the systemic inflammatory conditions, venous congestion, or pe- distribution of the TN and its branches. Sensory testing of distal ripheral edema, which often can be managed by addressing the sensory branches using the Semmes-Weinstein monofilaments systemic illness. Occasionally, vitamin B6 may reduce symptoms. or two-point discrimination may support TN compromise. If Low-dose tricyclic antidepressants (TCAs), such as amitrypti- the patient complains primarily of symptoms related to specific line, may be used to decrease nerve irritability, but side effects activities, i.e., an athlete with pain during running, then it may may preclude their efficacy. Gabapentin or other antiepileptic be helpful for the patient to perform the activity which exacer- drugs may be effective. When TTS is due to tension on the TN bates the symptoms before the examination. On occasion, the from excessive pronation of the foot, then modification of 36 Surgical Management of Entrapment Neuropathies in the Foot, Including Indications and Outcomes AAEM Course activity or use of a medial longitudinal arch support or a stirrup and inadequate release of a portion of the nerve and its branches. brace may be sufficient to relieve symptoms.37 Should nonoper- The third group has no TN scarring and an incomplete release. ative management fail, then consideration may be given to sur- The authors subdivide the first group into cases that (1) never gical intervention.76 experienced temporary relief after the first surgery, (2) experienced temporary relief but then recurrence, or (3) became worse Operative. Surgical management of TTS involves release of the and developed new symptoms. flexor retinaculum. Typically, release included the TN and its branches. The tarsal canal should routinely be explored to ensure Evaluation that no masses are responsible for nerve compromise. Neurolysis is not typically performed because doing so may make the nerve Diagnosis is typically made based on history and physical exam- more vulnerable to scarring by disrupting its surrounding bed ination.115 The history is usually consistent with recurrent or and damaging its blood supply. new symptoms described for TTS. Knowledge of the mechanism of injury may also be helpful. If there was a space-occupy- Results ing lesion or there had been repetitive trauma, entrapment or an external nerve compression may have been the primary diagno- Several authors have stated that nonoperative management of sis. However, if a crush or stretch injury was noted, the primary TTS is only palliative;35,73,75 however, if a dynamic cause of TN problem may not have been an external nerve problem but an stretch can be identified, then correction of malalignment with internal nerve disorder that may never respond to a release. An use of an orthosis is sometimes successful.19,50,76 Rarely, corticos- important component of the history is a review of the character teroid injection of the tarsal canal is successful in maintaining of the symptoms before previous tarsal tunnel release and a improvement of symptoms.19,50 Tarsal tunnel syndrome due to review of the previous operative report. This information may be space-occupying lesions responds poorly to nonoperative man- useful in defining incomplete previous release or incorrect diag- agement.19 nosis. A history of wound compromise or infection after the initial release is suggestive of new entrapment of the nerve or ad- Review of the literature suggests that surgical tarsal tunnel release hesive neuralgia. results in approximately 60-91% satisfactory results.19,23,50 Results appear to be best when a space-occupying lesion is iden- Although pain may be poorly localized, physical examination tified and removed.76 In the current authors’ experience, results should attempt to find foci of maximum involvement, specifi- are unpredictable when there is no underlying systemic neu- cally with regard to proximal or distal areas of symptoms. ropathy or when the symptoms are exacerbated spontaneously Percussion paresthesias over the scar of the TN release often may without provocation (ectopic neuralgia). be indicative of scar formation around the TN, whereas similar findings more distal or proximal to the old incision suggest in- Recurrent Tarsal Tunnel Syndrome complete decompression. A more focal point of paresthesias may indicate a neuroma or neuroma in continuity. A zone of numb- Overview/Etiology ness surrounded by increased nerve sensitivity with proximal trigger points suggests a deafferentation phenomenon, a sign of Previous reports suggest that symptoms may persist in 9-25% of nerve transection. Anesthesia dolorosa or a numb zone that is patients undergoing tarsal tunnel release or recur at variable time painful to touch is also indicative of nerve transection and periods after decompression.19,23,75,76,94,129 Persistent or recurrent neuroma. Decreased and painful range of motion and a thick- pain after previous tarsal tunnel release represents a management ened scar are consistent with adhesive neuralgia. Occasionally, dilemma. Persistence of symptoms may suggest incomplete recurrent or persistent symptoms are associated with vasomotor release, incorrect diagnosis (i.e., nerve not entrapped in tarsal instability; changes in skin temperature, color, or hair; sweating tunnel, more proximal etiology, neuroma in continuity, or true or dryness; sympathetically mediated pain; or chronic region neuroma), systemic neuropathy, or poor technique (i.e., exces- pain syndrome (type II). In these situations, the sympathetic sive nerve trauma during surgery). Recurrence generally is in- system should be addressed initially by sympathetic blockade dicative of scar formation resulting in nerve dysfunction. It has (via medications or injections) to identify the TN compromise been found useful to separate the cases into three categories, fa- by distinguishing between the reactive sympathetic symptoms cilitating management and permitting a more predictable and the primary nerve symptoms. outcome.115 The classification scheme is based on the presence of scar tissue about the TN and the adequacy of decompression of As in primary TTS, EDX studies may be of benefit especially to the trunk and the affected distal branches. The first group com- localize the nerve pathology, to identify transected nerve prises TNs encased in scar tissue and adequate distal release branches, and to distinguish between external nerve entrapment based on operative report or length of scar. The second group and internal nerve damage. For example, when conduction consists of a combination of TN branches encased in scar tissue delays are found, the diagnosis of entrapment is supported. AAEM Course Painful Foot and Ankle 37

Evidence of axonal damage and muscle denervation are sup- rarely results in complete satisfactory improvement of symp- portive of intraneural damage (i.e., neuroma or neuroma in con- toms. tinuity).111,115 Although only limited data are available, MRI has been shown promise in identifying factors leading to failed tarsal Results of revision TN release without vein wrap, transection, or tunnel release.129 stimulation can be stratified according to three categories.115 Outcome for neurolysis alone is typically poor when the TN is Management encased in scar tissue or when the pathology is a neuroma or neuroma-in-continuity.76,115 Some relief of symptoms can be an- Nonoperative. Nonoperative management of persistent or re- ticipated when the distal release is revised secondary to inade- current TTS may be extremely challenging. With persistent or quate decompression.115 The best results are found in patients in recurrent symptoms, the patient has typically failed nonopera- whom persistent or recurrent symptoms are due to inadequate tive measures before primary release, and thus it is unlikely that previous distal release alone.76,115 The results of transection, nonoperative measures will alleviate continued symptoms. wrap, or peripheral nerve stimulation are discussed below. The However, NSAIDs, TCAs, antiepileptic medications, orthotics, authors’ reported experience with more than 147 revision surg- and physical therapy/desensitization (transcutaneous electrical eries for such patients is that vein wrap for adhesive neuralgia, re- nerve stimulation [TENS] unit) should be attempted before per- vision transection for tibial branch neuromas, and peripheral forming revision surgery. Input by pain specialists, who can nerve stimulation for anesthesia dolorosa, ectopic neuralgia, provide insight into other effective means of pain control, should deafferentation pain, and the nerve subjected to multiple surg- be considered. A multilodality approach is often warranted. eries have resulted in 80% of the patients realizing 40-50% improvement in pain and function.34,111 Operative. The goal of revision surgery is to achieve pain relief and improve function. Options for revision surgery include revision release, revision release with barrier procedure, revision MEDIAL PLANTAR NERVE ENTRAPMENT (JOGGER’S FOOT) release with transection and burial of a neuroma, and peripheral or spinal cord stimulator. The best indications for revision release Overview/Etiology/Anatomy are usually limited to inadequate previous release with focal areas of nerve irritability.59,76,111,129 Proximally, the TN should be dis- Rask95 introduced the term “jogger’s foot,” referring to isolated sected free from scar tissue, and distally the abductor hallucis MPN entrapment between the deep fascia of the ABH and the (ABH) fascia should be released to allow for decompression of navicular tuberosity as it courses from beneath the flexor reti- the MPN, LPN, and FBLPN.76,115,129 Occasionally, preoperative naculum toward the master knot of Henry. Typically this syn- assessment suggests involvement of the MCN, which should drome is associated repetitive stress of the nerve in runners or also be released. Neuromas should be identified and transected military recruits, often with excessive hindfoot valgus and hy- more proximally and/or buried into fat, muscle, or bone. If the perpronation of the foot.85,117 Although medial arch supports TN has been transected, a cable graft or vein tube graft may be may improve foot alignment, they may exacerbate symptoms by considered. In the presence of adhesive neuralgia, revision release further compressing the MPN.108 with a barrier procedure, such as a vein wrap, is warranted. For a patient with ectopic neuralgia, anesthesia dolorosa, or deaf- Kopell and Thompson66 theorized that MPN entrapment is as- ferentation phenomenon, neurostimulation should be consid- sociated with hallux rigidus, as the patient attempts to lift the ered. For a patient with diffuse nerve symptomatology, especially arch with tibialis anterior overactivity. Furthermore, denervation one who does not respond to a nerve block, spinal cord stimula- of the forefoot in the distribution of the MPN by this mecha- tion is preferable to peripheral neurostimulation. Patients with nism led to greater hallux metatarsophalangeal (MTP) joint de- severe focal TN involvement are candidates for peripheral nerve generation.66 Although possible, this relationship has not been stimulation. Should a major component of sympathetically me- substantiated by any other study. diated pain be apparent, then surgery and postoperative management should include the use of a continuous sympathetic Evaluation block via epidural catheter. History Results Patients are typically runners with medial arch pain that radiates Results of the management of persistent or recurrent TTS have to the medial three toes.76,108 Occasionally, pain also radiates received little attention in the literature. Reoperation in patients proximally to the medial ankle. The patient may state that with recurrent or persistent symptoms after tarsal tunnel release he/she uses orthotic devices for running and that the onset of 38 Surgical Management of Entrapment Neuropathies in the Foot, Including Indications and Outcomes AAEM Course symptoms coincided with the use of a new device.76 Symptoms Results are typically related to specific activities, especially running, and are relieved by rest.109 No large series of isolated MPN releases is available. Our experience, and that of others, suggests that when history and physical Physical Examination examination are consistent with symptoms localized to the MPN, then isolated MPN decompression is successful in reliev- The patient should be viewed in a weightbearing position to ing medial arch pain.76 identify hindfoot valgus and hyperpronation of the foot. The patient should also be examined standing on his/her orthotic device to identify any areas of external compression. Palpation LATERAL PLANTAR NERVE ENTRAPMENT along the MPN usually reproduces symptoms, consisting of medial arch tenderness and radiation of dyesthesia or paresthesia Isolated LPN entrapment in the tarsal tunnel is rarely discussed; to the medial three toes. Symptoms may be increased with tight- in the literature, LPN compromise is typically considered as part ening of the ABH muscle, which can be accomplished with a of TTS or as an FBLPN entrapment (discussed below). heel rise or eversion of the heel. Because of the close proximity However, Kaplan and Kernahan59 noted that the LPN may be of the MPN and the toe flexors, distinguishing between neural- most vulnerable to entrapment in the tarsal canal because of its gia and tendinitis may be difficult. Usually, tenosynovitis is iden- oblique course in a separate tunnel under the ABP hallux. tified by forced toe plantarflexion against resistance or passive Electrodiagnostic studies for tarsal tunnel have supported this hyperextension, which should not produce neurologic symp- finding, because conduction compromise in TTS most fre- toms.108 Occasionally, it may be necessary to have a patient run quently involves the LPN fibers.9 on a treadmill for several minutes to identify symptomatology.109 First Branch (“Baxter’s Nerve”) Diagnostic Studies Overview/Etiology/Anatomy Weightbearing radiographs define the bony architecture and possibly may perinavicular arthritis or loss of medial column Although TTS may produce symptoms in the distribution of the alignment. These latter two findings suggest primary muscu- FBLPN, entrapment of the FBLPN should be viewed as an in- loskeletal pathology as the etiology of the symptoms. dependent entity.6,53,107 The close proximity of this nerve to the Electrodiagnostic studies may be helpful in identifying medial plantar fascia has implicated FBLPN compression as being re- plantar neuralgia, but because the syndrome is dynamic, such a sponsible for symptoms in 10-20% of patients with chronic heel static study typically contributes very little to the assessment. pain.6-8,112 Electrodiagnostic evaluation may detect a more proximal compression that has produces MPN symptoms.108 The FBLPN travels obliquely between the deep fascia of the ABH muscle and the quadratus plantae (QP), after which it Management courses laterally to separate into three branches, which supply the medial calcaneal periosteum, the flexor brevis, and the ab- Nonoperative ductor digiti quinti. The branch to the medial calcaneal periosteum has been shown to also innervate the QP. Entrapment Activity modification and accommodative shoe wear are usually typically occurs between the ABH and the QP, but it has also recommended in nonoperative management of medial plantar been noted where the nerve traverses the long plantar ligament neuralgia. Orthotic device modification may provide the neces- or the flexor digitorum brevis. Compression may be exacerbated sary medial support without aggravation of nerve symptoms. by hyperpronation of the foot, ABH hypertrophy, accessory Shoe modifications may compensate for hyperpronation so that musculature, or aberrant bursa formations.6,8,22,52,102 a lower arched device may be used.108 Occasionally, NSAIDs and cortisone injection may alleviate symptoms.108 Evaluation

Operative History. The patient typically complains of activity-related chronic heel pain that may radiate to the lateral aspect of the foot When symptoms are isolated to the MPN, decompression of and/or the medial ankle. The pain is exacerbated by activity, but only the MPN can be performed. Medial plantar nerve release is may be present with the first step in the morning or after rest. achieved by release of the ABH fascia and naviculocalcaneal lig- The pain will have a neuritic character that distinguishes it from ament at the level of the knot of Henry.76,108 the more common plantar fasciitis. When the two conditions AAEM Course Painful Foot and Ankle 39 coexist, it is difficult to separate the two entities.76 Patients fre- deep fascial layers of the ABH, but also partial medial plantar fa- quently report a history of ineffective management with heel sciectomy.6,8,76,108 Manipulation of the FBLPN should be pain protocols, including NSAIDs, heel cord stretching, heel avoided because it is sensitive to palpation and there may be in- pads, and corticosteroid injections. advertent damage to its accompanying fragile vein.

Physical examination. As with all peripheral nerve dysfunction, Results more proximal compromise should be ruled out with evaluation of low back pain, the sciatic nerve, and the TN. Although Results of surgical decompression of the FBLPN suggest satis- chronic heel pain symptoms may be diffuse or vague, an under- factory symptomatic relief of chronic heel pain in approximately standing of the anatomy of the medial and plantar heel fre- 85% of patients.6,8 In cases where evaluation suggests a contri- quently permits the examiner to distinguish between symptoms bution of the symptoms from more proximal TN compression, related primarily to nerve entrapment and those related to me- a more extensive tarsal tunnel release should be performed in ad- chanical symptoms of plantar fasciitis. The most common sites dition to this distal decompression.9 of nerve entrapment between the ABH, QP, and the flexor digitorum brevis are located proximal to the typical location of ten- Calcaneal Branches derness of the plantar fasciitis.9,76,108 Symptoms may be reproduced by everting the foot. Occasionally, weakness of the Overview/Etiology/Anatomy adductor digiti quinti may be apparent. In distinction to calcaneal stress fracture, FBLPN entrapment does not produce ten- The medial calcaneal branches of the TN provide sensation on derness to palpation over the lateral wall of the calcaneus or over the medial aspect of the heel. Anatomic studies have demon- the posterior calcaneal tuberosity. strated a proximal origin of the MCN branches from the TN and the existence of multiple MCN branches;25,28,51 one study Diagnostic studies. Anesthetic nerve blocks may be adminis- showed that 70% of MCNs originated proximal to the tarsal tered, but they offer little information in distinguishing between tunnel and that 60% of specimens had multiple branches.25 mechanical symptoms of plantar fasciitis and nerve symptoms Compromise of the MCN branches may contribute to chronic related to the FBLPN. Electrodiagnostic studies, however, have heel pain.9,54,100,123 The MCN branches do exhibit a considerable proven useful in the evaluation of chronic heel pain. Schon and amount of variation in terms of location, origin, and course. An colleagues112 demonstrated that needle EMG or NCSs are sensi- MCN may occasionally originate from the MPN.25,51,112 tive in detecting plantar nerve functional abnormalities in patients with chronic heel pain. A technetium bone scan will Some studies have demonstrated that calcaneal “neuromas” may frequently show plantar medial tuberosity uptake with plantar produce a painful heel syndrome;21,24,41 however, most likely fasciitis or calcaneal stress fracture. such a painful heel syndrome secondary to MCN compromise occurs only when a true MCN neuroma resulted from a tran- Management section injury during previous surgery.112 With an accessory muscle (i.e., soleus or flexor hallucis longus), we have seen symp- Nonoperative. Nonoperative management is essentially the tomatic tenting of the MCN over the bulky muscle. same as that for TTS. However, because of the overlap with mechanical symptoms, patients are typically treated for plantar Evaluation fasciitis as well. Corticosteroid injections may prove to be beneficial not only for plantar fasciitis but also in reducing inflam- Confirmation of MCN compression cannot be achieved by mation contributing to nerve irritation.108 An ankle/foot standard EDX studies because the MCN is a pure sensory nerve. orthosis worn at night may sometimes be beneficial.127 Typically, Testing methods that rely on the patient sensing and expressing nonoperative management is effective in treating chronic heel skin sensitivity to two-point stimulation or irritation may help pain, although symptoms may persist for more than a year objectify the findings. An accessory muscle or space-occupying despite continued nonoperative measures. lesion can be appreciated on computed tomography or MRI scan. Operative. For recalcitrant heel pain that has not improved after 6-12 months of nonoperative management, consideration may Management be given to surgical intervention, especially in the presence of a positive EDX correlation. The operative procedure involves not As with other syndromes, nonoperative techniques can be used. only decompression of the nerve by release of the superficial and When these fail, surgical management may be considered. 40 Surgical Management of Entrapment Neuropathies in the Foot, Including Indications and Outcomes AAEM Course

Typically, release of the tarsal tunnel with careful release of the space.77 The equal frequency of second and third interdigital MCN is performed. When there is an accessory muscle in- neuromas is supported by a cadaveric study which demonstrated volved, resection of the bulky distal portion is suggested. that the ratios of intermetatarsal head distances to the digital nerve diameters were significantly less in the second and third Results web spaces compared with the first and fourth web spaces.71 In rare instances, both the second and third web spaces may be in- In the authors’ experience with a limited number of cases of volved concurrently.10,30 Interdigital neuralgia very rarely occurs MCN entrapment, good to excellent results can be expected in the first and fourth web spaces.128 Several theories have been 75% of the time. When the nerve has been previously tran- proposed to account for the higher incidence of third web space sected, a more proximal transection and burial is often difficult, neuralgia, most of which have an anatomic basis. Several reports and a centrocentral anastomosis, vein graft, or PNS may be war- suggest that the confluence of medial and lateral nerve fibers ranted.44,111 creates greater thickness of the third interspace common digital nerve, predisposing it to irritation,11,58 a theory that has been refuted by the same cadaveric study noted above.71 Other INTERDIGITAL NEURALGIA (“MORTON’S NEUROMA”) authors have suggested that the relative mobility of the lateral column of the foot compared with the more immobile medial Overview/Etiology/Anatomic Considerations column creates stress on the third common digital nerve.76 However, this theory does not explain the occurrence of a con- The term neuroma is probably a misnomer, because it generally siderable number of second web space neuralgias.77 refers to interruption of nerve fibers. Interdigital neuralgia, or nerve-related pain, is a more appropriate term for painful afflic- As pointed out by Mann and Baxter,76 etiologic considerations tions of the common digital nerve. This condition was first de- can be separated into anatomic, traumatic, and extrinsic factors. scribed by Durlacher in 1845,33 but it was not until 194011 that Besides the anatomic factors discussed above, the plantar loca- it was considered an entrapment phenomenon caused by the tion of the common digital nerve predisposes it to direct injury. nerve being stretched over the edge of the intermetatarsal liga- Extrinisic factors involve any adjacent structures that may con- ment and anterior edge of the coalesced portion of the plantar tribute to nerve entrapment or compromise. Mann and Baxter76 fascia. Morton82 theorized that the nerve is compressed between have described thickening of the transverse metatarsal ligament, the metatarsal heads. Anatomic studies have proved that this is which may cause nerve compression even without hyperdorsi- not the mechanism responsible for symptoms because the inter- flexion of the MTP joints. Mass effects may occur with ganglia digital nerve courses plantar to the transverse intermetatarsal lig- or tumors, such as lipomas, in the web space. Deviation of the ament and the metatarsal heads. MTP joint due to attenuation of the capsule may diminish the web space or even create traction on the digital nerve. A hyper- The theory of transverse intermetatarsal ligament compression mobile first ray in runners may result in transfer metatarsalgia of the nerve is supported by studies demonstrating that histo- and transfer calluses under the lesser metatarsal heads, creating logic neural changes occur distal to the transverse metatarsal lig- pressure on the common digital nerves. Inflammation in the ament, while neural anatomy proximal to the ligament appears web space may also create nerve compromise. An intermetatarsal normal.46 Specific histologic findings include amorphous bursa has been described by several authors;4,13 it may become eosinophilic material deposition and gradual nerve fiber degen- inflamed, whether or not it is associated with rheumatologic eration. The entrapment phenomenon may be exacerbated by conditions. Typically it is not the mass effect of the bursa, but high-heeled shoes because hyperextension of the MTP joints instead the associated inflammation that is responsible for nerve causes greater tethering of the nerve by the transverse metatarsal dysfunction. Finally, synovitis of the adjacent MTP joint may ligament.76 Such stress on the nerve may account for an in- create inflammation that clinically manifests as interdigital neu- creased incidence of interdigital neuralgia in women. A similar ralgia.17 tethering of the nerve around the transverse metatarsal ligament may occur in athletes involved in activities requiring MTP joint Interdigital neuralgia must be distinguished from other causes of hyperextension (i.e., dancers en pointe or runners rolling plantar forefoot pain, although, as noted above, some forms of through the forefoot).76,109 interdigital neuralgia are a result of adjacent forefoot pathology. The differential diagnosis includes metatarsalgia, MTP joint dis- Most authors have found that interdigital neuralgia is most orders (including degenerative changes, instability, synovitis, in- common in the third web space,11,49 but others state that the flammatory conditions), metatarsal stress fracture, and more condition occurs with equal frequency in the second web proximal nerve compromise. AAEM Course Painful Foot and Ankle 41

Evaluation sound97,114 and MRI36,124 have been shown to aid in the diagnosis of interdigital neuralgia, another recent study suggested a high History false negative rate when these imaging techniques are correlated with surgical findings.98 As these imaging techniques evolve, Patients with interdigital neuralgia typically complain of activity- they will most likely contribute substantially to confirming clin- related plantar foot pain between the metatarsal heads. Although ical suspicion when necessary. Electrodiagnostic studies con- a sharp pain or an ache may be present, the pain is generally tribute little in the assessment of true interdigital neuralgia, but burning in nature, radiating into the toes. Occasionally, the pain needle EMG and NCSs may elucidate a contribution to the pain may radiate proximally to the ankle or produce numbness in the pattern from a proximal nerve compromise. toes. A characteristic finding is that the pain is aggravated by weightbearing, especially in tight toebox or high-heeled shoes, A helpful diagnostic test is a web-space injection of an anesthetic, and relieved by rest and removal of shoes. As with all the en- inferior to the transverse metatarsal ligament. Relief of symp- trapment syndromes, a history of low back pain or pathology toms from an accurate injection frequently confirms the diagno- should also be documented to ensure that symptoms are not sec- sis of interdigital neuralgia. ondary to radiculopathy or created by a double-crush phenomenon. Management

Physical Examination Nonoperative

The objective of a physical examination is to identify findings Nonoperative management consists of elimination of any factors consistent with and responsible for interdigital neuralgia and to that may be contributing to nerve compromise. Wider toebox rule out other diagnoses that may be producing plantar foot shoes, reduction of shoe heel height, softer soled shoes or inserts, symptoms. The patient’s foot should be observed in the weight- and activity modification often prove to be beneficial. Metatarsal bearing position to appreciate any deformity such as toe pads may reduce distal pressure between the metatarsal heads, malalignment or web space fullness. Range of motion and stress but occasionally they exacerbate symptoms by creating more testing of the MTP joints may suggest degenerative change, syn- proximal pressure on the common digital nerve. Diagnostic ovitis, or instability contributing to or mistaken for neural- anesthetic blocks may be combined with corticosteroid injec- gia.4,88,128 Palpation of the web space may occasionally suggest a tions, which have been shown to provide long-term relief of mass effect such as a ganglion or lipoma; however, such findings symptoms in some patients. However, in patients with symp- are rare. Palpation of the affected plantar interspace(s) typically toms caused by malalignment of the MTP joints, multiple cor- reproduces symptoms consistent with neuralgia; tenderness of ticosteroid injections may lead to additional attenuation of the the metatarsal heads suggests metatarsalgia and is not indicative joint capsule and increased nerve compromise. Also, corticos- of neuralgia. A Mulder’s sign84 is an excellent test in the evalua- teroids may create fat pad atrophy, leading to more pressure on tion of interdigital neuralgia. The test is performed by concur- the common digital nerve. rently applying web space pressure distal to the metatarsal heads and compressing the metatarsal heads transversely. A positive test Operative is documented when a “click” is appreciated and the patient’s symptoms are reproduced. The click probably represents plantar Surgical intervention is considered for patients who have failed displacement of tissues between the metatarsals with subsequent nonoperative management. An important diagnostic and prog- impact on impingement on the nerve. However, a click without nostic tool is web space injection of an anesthetic; if complete reproduction of symptoms is not diagnostic of interdigital neu- relief of symptoms is achieved, then nerve resection most likely ralgia. The course of the TN from proximal to distal should be will be successful in diminishing the patient’s pain. Surgical palpated. Although tenderness is usually at or distal to the treatment in patients with more proximal common digital nerve metatarsal heads, more proximal tenderness may be indicative of tenderness or with tarsal tunnel tenderness may require addi- a less focal process. Rarely is decreased sensation noted in the tional surgical decisions. When the nerve is tender at or proxi- toes affected by the nerve compromise. Finally, as mentioned mal to the metatarsal heads and web site injection at this site previously, evaluation should also include examination to rule alleviates the pain, then resection at that level would be consid- out radiculopathy. ered.

Diagnostic Studies Interdigital nerves can be approached from dorsal77 or plantar incisions.11,60,90,99 The most commonly described technique in- Weightbearing plain radiographs may define malalignment such volves a dorsal approach through a longitudinal incision with as splay or claw toes or degenerative changes of the forefoot. transection of the intermetatarsal ligament and proximal neurec- Rarely, radiographs may reveal a foreign body. Although ultra- tomy. Current recommendations favor neurectomy 3 cm proxi- 42 Surgical Management of Entrapment Neuropathies in the Foot, Including Indications and Outcomes AAEM Course mal to the intermetatarsal ligament to ensure that all plantar nerves, or bilateral nerves yields less favorable results. Transection nerve branches are included in the resection.3,128 Other authors of the intermetatarsal ligament without neurectomy has been re- have described a plantar approach through either longitudinal ported to yield approximately 80-85% satisfactory results.27,30,40 incisions between the metatarsal heads or transverse incisions Additional study of patient selection factors and results with this proximal to the metatarsal heads.11,60,90,99 Plantar approaches technique are warranted. may result in a painful scar if performed under or distal to the metatarsal heads and longitudinal plantar incisions frequently create fat pad atrophy and chronic metatarsalgia due to scar hy- RECURRENT INTERDIGITAL NEURALGIA perkeratosis. Richardson and colleagues99 reported favorable on the plantar approach, but observed that wound drainage, plantar Overview/Etiology keratosis, and scar tenderness were the most common complications. A transverse incision proximal to the metatarsal heads Recurrent or persistent interdigital neuralgia is often the results allows for adequate exposure for nerve resection and avoids in- of an incorrect diagnosis rather than a true recurrence.57,76 A terference with the metatarsal heads during weightbearing. more proximal nerve compromise may contribute to the interdigital symptoms, either completely or as part of a double-crush Several authors have recommended dorsal approach for trans- phenomenon; therefore more proximal areas of compression verse metatarsal ligament transection without neurectomy,27,30,40 should be identified. Occasionally, the incorrect web space may treating the condition as an entrapment syndrome. Although be identified on initial examination, and the surgical procedure this procedure avoids potential recurrent or refractory plantar performed on the incorrect interdigital nerve.56,57 If the pathol- neuroma formation because neurectomy is not performed, there ogy truly was at the web space, then persistent or recurrent is concern that several clinicians have observed reconstitution of symptoms may be secondary to inadequate proximal nerve re- the transverse intermetatarsal ligament.77,128 However, long-term section with neuroma formation in a weightbearing portion of follow-up with this technique suggests that this ligament recon- the forefoot3,10,56,57,76 or inadequate intermetatarsal ligament stitution is probably not clinically significant.40 release. Mann and Reynolds77 and Mann and Baxter76 have also observed an accessory branch or traumatic neuroma that is fre- Postoperatively, a patient is placed in a postoperative shoe and quently missed at the time of primary nerve resection and which may bear weight on the heel. At 2 weeks, sutures are removed. remains under the metatarsal head after resection of the remain- Patients may progress with activity as tolerated but are instructed der of the nerve. that there may be flares of nerve symptoms for several months. Surgical excision of an interdigital nerve obviously results in Evaluation numbness between the affected toes; it is advisable to inform patients of this preoperatively. History

Results Because recurrence or persistence of interdigital neuralgia after surgical resection is frequently due to misdiagnosis, evaluation as It has been estimated that only 20% of patients experience com- described for virgin interdigital neuralgia should be repeated.10,76 plete resolution of symptoms of interdigital neuralgia with non- To administer appropriate management, it is essential to localize operative measures alone.46 Results of corticosteroid injection symptoms, and a review of preoperative symptoms is often suggest that although most patients gain temporary relief of helpful.76 History should include whether or not the patient had symptoms, symptoms are rarely eliminated completely. a symptom-free interval with weightbearing after primary nerve Greenfield and colleagues47 suggested that, in a series of steroid resection. Any associated symptoms, such as radiation of pain injections for suspected interdigital neuralgia, only 30% of pa- from the ankle, leg, or back, should be noted.10 tients had substantial relief over a 2-year period. More recently, Rasmussen and colleagues96 noted that although most patients Physical Examination with third web space neuralgia had relief of symptoms with a single steroid injection, most were still symptomatic. Of the 51 Physical examination of the forefoot may reveal a localized area feet in the study, 50% underwent subsequent surgical resection of tenderness and a positive Tinel’s sign, suggestive of a stump with 96% success; the other 50% remained symptomatic. neuroma.3,57,128 Palpation of the metatarsal heads may be suggestive of an accessory nerve branch (as described by Mann and Reports of common digital nerve resection for failed nonopera- Reynolds77 and Mann and Baxter76) or other bony pathology tive management of interdigital neuralgia suggests satisfactory that may be creating nerve impingement. Other forefoot pathol- relief of symptoms in 80-96% of patients.38,77,96 Results appear ogy may be responsible for the pain, and thus other sources of to be best for isolated third web space neuralgia. Resection of iso- symptoms should be identified, such as MTP joint synovitis or lated common digital nerves other than the third, multiple metatarsalgia. Occasionally, interdigital neuralgia is found in ad- AAEM Course Painful Foot and Ankle 43 jacent web spaces.57 Examination of the tarsal tunnel, lower ex- In a small series of patients, Mann and Reynolds77 and Mann tremity, or the back may unmask areas of more proximal com- and Baxter76 observed that 81% of patients were asymptomatic pression contributing to interdigital symptoms. and 18% were either marginally or not improved after revision surgery through a dorsal approach. Diagnostic Studies

Plain radiographs should be obtained to ensure that no bony ab- SUPERFICIAL PERONEAL NERVE ENTRAPMENT normalities are present that may be responsible for continued nerve compression. Other imaging studies such as MRI or ul- Overview/Anatomy trasound may be suggestive of nerve pathology, but scar tissue from the previous surgical procedure may obscure interpreta- Entrapment of the superficial peroneal nerve (SPN) is not tion. A repeat diagnostic anesthetic block in the affected web common.22,74,80,119 Although it may occur idiopathically, this space may be useful in identifying residual or recurrent distal clinical entity is typically associated with ankle instability,65,74 nerve pathology. Occasionally, evaluation of a neuropathy is in- direct trauma (with associated ganglion),67,116 fibular fracture,9 dicated, including blood tests, nerve studies, or MRIs of the exertional compartment syndrome (and previous fas- spine. ciotomy),119,120 muscle herniation,39,80 lower extremity edema, and (rarely) mass effects such as tumors.5 Probably the most Management meaningful association is that of chronic ankle sprains and persistent postinjury anterolateral ankle pain.108 Results of management of recurrent or persistent interdigital neuralgia are typically less successful than those for primary in- Anatomic considerations are important. After branching from terdigital neuralgia.10,57 Nonoperative management should be re- the common peroneal nerve, the SPN usually courses in the peated, as for a primary interdigital neuralgia with lateral compartment of the leg. It passes through a deep fascial accommodative shoe wear, metatarsal supports, NSAIDS, and tunnel approximately 8-12 cm above the lateral malleolus, after possibly a cortisone injection.10,77 Physical therapy desensitiza- which the nerve divides further into medial and intermediate cu- tion modalities may prove beneficial. taneous branches.1,119 The medial branch supplies sensation to the dorsomedial aspect of the ankle and foot, whereas the inter- As with primary interdigital neuralgia that has failed nonopera- mediate branch is responsible for sensation over the dorsocentral tive management, the approach may be dorsal14,77 or plantar10,57 aspect of the ankle and foot.106 The fibrous tunnel is a site of po- in revision surgery. Proponents of the dorsal approach cite a tential nerve entrapment, as is muscle herniation through the concern for plantar wound complications;77 those preferring a fascial aperture where the nerve leaves the compartment.119 Such plantar incision state that the plantar approach allows for greater herniation may only occur in the dynamic state and be part of a proximal resection of the nerve and avoids dorsal scar tissue from localized “anterior exertional compartment syndrome.” Ankle the previous surgery.10,57 A transverse plantar incision can also be inversion instability may produce a traction injury to the inter- used, as in primary interdigital neuroma resection. mediate cutaneous branch, especially if the nerve is trapped at the site of exit from the deep fascia. Therefore, SPN entrapment Results should be considered in patients with chronic pain after ankle sprain. Occasionally, SPN neuralgia occurs after anterior com- Typically, nonoperative management of recurrent or persistent partment fasciotomy due to reorientation of the fascia, the nerve, interdigital neuralgia/neuroma is palliative.10,57 Mann and and the fibrous tunnel.119 Reynolds77 estimated successful nonoperative management to be between 10 and 20%. Results of revision interdigital nerve re- Evaluation section are less predictable than for primary procedure, with patient dissatisfaction with results after reoperation approaching History 40%.76,77 Beskin and Baxter10 reported that 80% of patients undergoing revision resection noted substantial improvement; Patients typically report pain, paresthesias, or numbness on the however, less than 50% gained complete relief of symptoms. In anterolateral ankle and foot. Occasionally pain will radiate into the series of Johnson and colleagues,57 67% of patients experi- the thigh.67 Approximately 25% of patients recall a history of enced complete relief of symptoms, and 24% had no improve- trauma,67,109 which generally is an ankle sprain. A history of an- ment or even worsening of symptoms. Most of the procedures terior compartment fasciotomy is also clinically significant, as for these two series were performed through a plantar approach. noted previously. 44 Surgical Management of Entrapment Neuropathies in the Foot, Including Indications and Outcomes AAEM Course

Physical Examination Operative

As with any neurologic evaluation of the lower extremity, more In isolated nerve pathology, operative intervention is directed at proximal areas of nerve compromise should be identified, and nerve decompression, which usually involves release of the nerve examination should rule out radiculopathy and entrapment of at the fibrous tunnel.65,74,80,119 A more extensive compartment the sciatic and common peroneal nerves. Ankle instability release can be performed to eliminate muscle herniation on the should be documented. Palpation of the SPN may identify a SPN.119 In the rare cases in which previous anterior compart- specific site of nerve irritation, muscle herniation, fascial defect, ment release has resulted in SPN, revision of the fascial release and/or bony prominences.109 Palpation of the nerve may and lateral fascial release may be required.119 Any mass effect of produce paresthesias in the distribution of the SPN. Usually, the exostoses should also be removed. When nerve compromise is problem can be localized to the area where the nerve exits from associated with ankle instability, then nerve decompression is the fascia.109,119 Styf118 described three provocative tests to aid in combined with lateral ankle ligament reconstruction.9 diagnosis of SPN entrapment once the site of nerve irritation is identified. The first test involves palpation of the nerve while the Results patient actively dorsiflexes and everts the ankle; the two other tests involve plantarflexion and inversion with and without pal- Results of nonoperative management are not extensively ad- pation at the site of nerve irritation. Findings from these tests dressed in the literature. It has been suggested that relief of symp- may be difficult to distinguish from mechanical symptoms in toms of long-standing SPN entrapment by nonoperative means patients with associated chronic ankle instability. Some patients is typically inadequate.108,109 However, it can be inferred that if may have decreased sensation distal to the site of maximum irri- SPN symptoms are secondary to dynamic causes, such as tation. chronic ankle instability, then stabilization will result in improvement of symptoms. Diagnostic Studies The largest series of SPN decompression suggests that improve- Plain radiographs may reveal fracture fragments or bony promi- ment of symptoms can be anticipated in 75% of cases, but it nences that may be responsible for symptoms.119 warned that results are less predictable in athletes.119 Case reports Electrodiagnostic studies may be useful in confirming areas of of SPN release have demonstrated effective relief of symp- SPN compromise suggested on clinical examination and are es- toms.65,74,80 pecially useful in diagnosing more proximal nerve compromise or peripheral neuropathy.119 Diagnostic anesthetic blocks may also confirm the diagnosis of SPN neuralgia.9,65,108 Should DEEP PERONEAL NERVE ENTRAPMENT (“ANTERIOR TARSAL history and physical examination suggest exertional compart- TUNNEL SYNDROME”) ment syndrome, compartment pressure measurements are performed.108,119 Overview/Etiology/Anatomy

Management Deep peroneal nerve (DPN) entrapment was initially described by Kopell and Thompson66 in 1960 and was designated an “an- Nonoperative terior tarsal tunnel syndrome” by Marinacci78 in 1968. The DPN branches from the common peroneal nerve and courses Nonoperative management is usually aimed at eliminating po- between the extensor hallucis longus and the extensor digitorum tential traction on the entrapped SPN with modalities typically longus just proximal to the ankle. Approximately 1 cm above the used in the treatment of ankle instability/sprains.9,108 Physical ankle joint, the nerve divides into a motor branch to the exten- therapy to strengthen the peroneal musculature, ankle bracing, sor digitorum brevis (EDB) and a sensory branch that continues and lateral shoe wedges have been described. An ankle/foot or- to the first web space. As this sensory branch crosses the ankle thosis in neutral worn at night may decrease SPN symptoms by and the dorsum of the foot, there are several sites of potential decreasing the stretch on the nerve. However, these modalities compression. Because the motor branch to the EDB is proximal need to be used cautiously. Vigorous strengthening of the per- to these sites of compression, the findings are typically related oneal musculature may further irritate the SPN at the fibrous purely to the sensory branch.26 Krause and colleagues68 described tunnel, and ankle braces may create external compression of the a “partial anterior tarsal tunnel syndrome” in which only the nerve fibers. Vitamin B6, NSAIDs, TCAs, and antiepileptic motor or sensory component was involved. The most frequently medications may reduce symptoms. Corticosteroid injections at described site of entrapment is between the inferior edge of the the site of nerve compromise may also diminish symptoms. extensor retinaculum and the talus and navicular, where these AAEM Course Painful Foot and Ankle 45 structures create a fibroosseous “anterior tarsal tunnel.”42,78,109 and testing for ankle instability. If the history is consistent with Entrapment may also occur at the superior edge of the extensor an anterior compartment syndrome, then examination should retinaculum, at which point the EHL tendon crosses the also be performed after exacerbation of symptoms on a tread- DPN,12,78 and also where the nerve is crossed by the extensor mill, with measurements of compartment pressures. hallucis brevis tendon.67 Trauma and degenerative changes have also been shown to contribute to deep peroneal neuralgia, and Diagnostic Studies/Tests dorsal osteophytes of the foot and ankle may be responsible for nerve compression.85,109 Although ankle instability is more com- Plain radiographs are useful in identifying exostoses or osteo- monly associated with SPN neuralgia, plantarflexion and phytes that may contribute to nerve compression. supination places the DPN under maximum tension, especially Electrodiagnostic studies may reveal areas of distal entrapment in the presence of an underlying talonavicular osteophyte.12,108 but are typically more helpful in identifying areas of more prox- External compression or certain aberrant postures may con- imal nerve compression or peripheral neuropathies.26 tribute to deep peroneal neuralgia. Tight shoe wear and ski boots Occasionally, nerve conduction studies assist in distinguishing have been implicated,42,68,72 as has prolonged plantarflexion between distal and proximal DPN compression within the ante- during sleep, which places the nerve under tension. Finally, gan- rior tarsal tunnel. A diagnostic nerve block may confirm clinical glions or tumors rarely create pressure on the DPN in the re- findings and, as noted previously, compartment pressures should stricted space of the anterior tarsal tunnel.109 be measured if anterior compartment syndrome is suspected.

Evaluation Management

History Nonoperative

Patients with deep peroneal neuralgia complain of dorsal foot Nonoperative measures include use of accommodative shoe wear pain that may radiate to the first web space. As with other nerve that eliminates external compression on the dorsal ankle and symptoms of the foot and ankle, a history of low back pain foot and activity modification to avoid activities that exacerbate should be documented. If the symptoms are aggravated by ac- symptoms. As for SPN neuralgia, ankle braces may alleviate tivity or exercise, then consideration must be given to exertional nerve pain related to ankle instability but may potentially worsen compartment syndrome. Symptoms related to tight shoe wear or symptoms if external pressure is created. Vitamin B6, NSAIDs, particular activities (such as sit-ups with the anterior aspect of TCAs, and antiepileptic medications may reduce symptoms, the ankles under a metal restraint) should be noted. A history of and corticosteroid injection at the site of nerve irritation may foot and ankle trauma or chronic ankle instability is also impor- also be beneficial. tant. Operative Physical Examination Surgical intervention involves decompression of the entrapped Palpation along the course of the DPN may identify an area of nerve by release of the extensor retinaculum. If possible, a prox- maximum nerve irritation, is usually in the area of the inferior imal portion of the retinaculum should be preserved to avoid extensor retinaculum.26 Palpation may also locate dorsal ankle “bowstringing” of the extensor tendons. Occasionally, the exten- and foot osteophytes and rarely a ganglion related to previous sor hallucis brevis tendon must be released. All osteophytes and trauma or degenerative change. Sensation in the first web space exostoses should be resected as well.108 If ankle instability is di- may be diminished. Areas of more proximal nerve compromise agnosed as a major contributing factor to deep peroneal neural- should be ruled out with examination of the lower spine, sciatic gia, then ankle ligament reconstruction may need to be nerve, common peroneal nerve. Weakness and/or atrophy of the considered. Finally, when anterior compartment syndrome has EDB muscle is suggestive of a complete anterior tarsal syndrome been identified, then consideration is also given to fasciotomy. or more proximal pathology.26 However, patients may have symptoms consistent with an anterior TTS with both motor and Results sensory nerve compression despite lack of EDB atrophy. This situation is secondary to an accessory EDB innervation from the Based on anecdotal experience, nonoperative management is SPN, noted in approximately 22% of patients.15,48,69 When successful when the external sources of compression or ankle in- symptoms are reported to occur in the dynamic state, the evalu- stability contributing to symptoms are eliminated. Infrequently, ation should include dorsiflexion and plantarflexion of the ankle cortisone injection is effective in treatment of deep peroneal neu- 46 Surgical Management of Entrapment Neuropathies in the Foot, Including Indications and Outcomes AAEM Course ralgia.26 Nonoperative management is generally inadequate Diagnostic Studies when symptoms are secondary to soft-tissue, osteophyte, or ganglion impingement.26 Rarely, plain radiographs may demonstrate a bony abnormality responsible for the saphenous nerve compression, but typically The experience of Dellon26 with 20 DPN entrapments managed physical examination will prompt radiographic evaluation. Soft- with surgical decompression suggests an 80% satisfactory tissue masses may be assessed with MRI or ultrasound. The most outcome. Poor results are typically related to internal nerve useful tool is the anesthetic block at the site of nerve compro- damage or neuropathies contributing to nerve compromise, in mise, usually in the subsartorial canal. Some clinicians have which case simple neurolysis usually proved ineffective.26 demonstrated that somatosensory evoked potentials may aid in diagnosis of saphenous nerve entrapment.32,125

SAPHENOUS NERVE ENTRAPMENT Management

Overview/Etiology/Anatomy Nonoperative management may involve activity modification if symptoms have a dynamic component. Cortisone added to the Saphenous nerve entrapment or neuralgia is not common. diagnostic nerve block noted previously may prove therapeutic. Typically, entrapment of this nerve occurs about the knee, but Treating saphenous nerve entrapment with therapeutic blocks because its terminal distribution is at the medial ankle and foot, has resulted in satisfactory relief of symptoms in 38-80% of pa- patients may present with medial distal lower extremity pain sec- tients.83,101 Surgical management requires release of the anterior ondary to compromise of this nerve. The saphenous nerve aspect of Hunter’s canal and dissection of the saphenous/sartor- courses with the superficial femoral artery after originating from ial nerve fibers from the surrounding fascial.67,125 the femoral nerve. It penetrates the subsartorial fascia approximately 10 cm proximal to the medial femoral condyle and then divides into the infrapatellar and sartorial or distal saphenous SURAL NERVE ENTRAPMENT branches. The sartorial component descends along the medial tibial border with the greater saphenous vein. Approximately 15 Overview/Etiology/Anatomy cm proximal to the medial malleolus, the sartorial or distal saphenous nerve separates into two branches: one that supplies The medial sural nerve and lateral sural nerve (peroneal com- sensation to the medial aspect of the ankle and one that inner- municating branch) combine to form the sural nerve in the vates the medial foot. Although entrapment or compression may distal third of the leg on the lateral aspect of the ankle.16,20,92 occur anywhere along the nerve’s course, the most likely site of Sural nerve innervation combines fibers from both the tibial and compromise is at the subsartorial fascia, just proximal to the SPNs. Just proximal to the ankle, two branches of the sural nerve medial femoral condyle. become apparent: the lateral branch, which occasionally anasto- moses with the SPN, and the posterior branch, which innervates Evaluation the lateral aspect of the heel.16 The posterior division continues inferior to the peroneal tendons to supply sensation to the lateral History foot over the proximal fifth metatarsal.16,70 This network of branches is responsible for sensation on the lateral foot, heel, and Because the nerve compromise may be proximal, it is important ankle.106 to identify any history of knee injury, knee or bypass surgery, or pain. Direct trauma anywhere along the course of the nerve may Sural nerve entrapment may occur anywhere along its course, be responsible for entrapment within scar tissue. but most commonly it is a result of ankle or lateral foot injuries.110 Recurrent ankle sprains,93,110 fractures of the calcaneal Physical Examination base of the fifth metatarsal,45,93 peroneal and Achilles’ tendon inflammation, edema, and ganglion formation have also been Although the patient may complain of medial ankle and foot identified as causes for sural nerve compression or injury.93,109 pain, point tenderness is typically located over the subsartorial canal proximal to the medial femoral condyle. Occasionally, hy- Surgery about the lateral heel and foot may result in iatrogenic perextension of the knee will produce distal symptoms. In iso- sural nerve pathology.62,63 The network of sural nerve branches lated saphenous nerve compromise, no motor deficits will be often warrants traction or transection of the sural nerve in the present. The entire course of the nerve should be palpated to surgical management of calcaneus fractures, ligamentous insta- identify any other sites of possible nerve compromise. bility, tendon pathology, or hindfoot arthritis. Even without AAEM Course Painful Foot and Ankle 47 direct sural nerve injury, surgery adjacent to the sural nerve may Management result in scar entrapment, leading to adhesive neuralgia.108 Nonoperative Evaluation Nonoperative management of sural neuralgia requires identifica- History tion of the etiology of nerve compromise. As for any peripheral neuralgia, any other source of nerve compromise, such as sys- Most patients with sural nerve disorders recall a history of ankle temic illness responsible for neuralgia or more proximal sites of injuries, typically acute or recurrent ankle sprains. Patients with nerve compression, needs to be addressed. Isolated sural neural- persistent pain after ankle sprains may note radiating symptoms gia may respond to NSAIDS, TCAs, antiepileptic medications, or paresthesias associated with instability. Although the pain or vitamin B6. If nerve compromise is secondary to traction from pattern may be poorly localized, occasionally a focus of pain chronic ankle instability, then bracing, orthotics, or shoe modi- allows for identification of a specific area of nerve compromise fications may prove effective, as for SPN neuralgia. Caution with along the course of the sural nerve.109 Previous surgery on the bracing is advised because external compression may aggravate lateral heel and ankle (i.e., for a calcaneus fracture, lateral ankle sural nerve symptoms. Again, symptoms failing management of reconstruction, etc.), should be documented. the sural nerve may respond to treatment directed at the SPN, given the cross-innervation. Physical Examination Operative An understanding of sural nerve anatomy is essential in identifying areas of nerve entrapment from the popliteal fossa to the When a specific site of nerve compression, i.e., scar entrapment lateral foot. The overlap of the SPN and tibial peripheral nerve or local mass effect, identified on physical examination fails to fibers comprising the sural nerve may render the distal sensory respond to nonoperative management, then neurolysis may be examination unremarkable, despite symptoms suggesting en- effective in relieving symptoms.45,93 In rare situations, neurolysis trapment. A Tinel’s percussion test may be useful in localizing may involve decompression of SPN fibers as well. Should symp- foci of nerve compromise; often such findings are associated toms be related to ankle instability, then surgical stabilization with lateral heel/ankle surgical scars. may eliminate the dynamic etiology of sural neuralgia.110 Neuroma of the nerve may warrant higher transection and burial In the static situation, symptoms may not be observed when into muscle, fat, or bone. ankle instability is responsible for sural nerve entrapment pain. Examination should include inversion testing of the hindfoot Results and ankle to identify dynamic etiologies of sural neuralgia. As for other peripheral nerve compromise, consideration must be given No large series reporting the results of management of sural neu- to the double-crush phenomenon126 with evaluation of the ralgia is currently available. Anecdotal experience and case entire leg and lumbar spine. reports suggest that occasionally nonoperative management is effective. Surgical decompression of mass effects (such as scar en- Diagnostic Studies trapment, ganglions, and avulsion fractures) typically results in satisfactory symptomatic relief.45,93,108 It has been our experience Plain radiographs should be obtained to rule out bony abnor- that sural neuralgia due to ankle instability is managed effectively mality that may contribute to nerve compression, and MRI may with lateral ankle stabilization, without directly addressing the be helpful when a soft-tissue mass effect is suspected. sural nerve. Electrodiagnostic studies can occasionally confirm a clinical suspicion of limited sural nerve conduction, but these tests are typically most useful in diagnosing more proximal sites of nerve SUMMARY compromise. Diagnostic nerve blocks are of some use in defining sural nerve entrapment symptoms. A nerve block more prox- Nerve dysfunction of the foot and ankle may involve the tibial, imal to the affected area that relieves symptoms lends support to saphenous, sural, and superficial and DPNs. The nerves may be clinical suspicions of peripheral sural nerve entrapment. An damaged chronically by repetitive stretching or repetitive contu- anesthetic nerve block failing to relieve symptoms suggests that sion. Acutely, the nerve can be stretched, contused, or transected. symptoms either are derived from SPN crossover fibers or may Any of these mechanisms can result in nerve entrapment with be secondary to a more proximal nerve compromise. In such sit- pain and dysfunction. Evaluating these conditions requires uations, it is prudent to perform a second selective nerve block knowledge of neural anatomy, coupled with a detailed history of the fibers contributed by the SPN. and physical examination. 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Diagnosis and treatment of Morton’s axonal transport induced by acute, graded compression of the rabbit neuroma. JAAOS 1996;4:328-335. vagus nerve. J Neurol Neurosurg Psychiatry 1980;43:690-698. 129. Zeiss J, Fenton P, Ebraheim N, Coombs RJ. Magnetic resonance 104. Sammarco GJ, Chalk DE, Feibel JH. Tarsal tunnel syndrome and ad- imaging for ineffectual tarsal tunnel surgical treatment. Clin Orthop ditional nerve lesions in the same limb. Foot Ankle 1993;14:71-77. 1991;264:264-266. 105. Sammarco GJ, Stephens MM. Tarsal tunnel syndrome caused by the flexor digitorum accessorius longus. A case report. J Bone Joint Surg CURRENT SUGGESTED READING Am 1990;72:453-454. 106. Sarrafian SK. Anatomy of the foot and ankle. Descriptive, topo- 1. Bennett GL, Graham CE, Mauldin DM. Morton's interdigital graphic, functional. Philadelphia: JB Lippincott Co; 1983. neuroma: a comprehensive treatment protocol. Foot Ankle Int 107. Schon LC. Plantar fascia and Baxter’s nerve release. In: Myerson M, 1995;16:760-763. editor. Current therapy in foot and ankle surgery. St. Louis: Mosby- 2. Coughlin MJ, Pinsonneault T. Operative treatment of interdigital Year Book Inc; 1993. p 177-182. neuroma. A long-term follow-up study. J Bone Joint Surg Am 108. Schon LC. Nerve entrapment, neuropathy, and nerve dysfunction in 2001;83:1321-1328. athletes. Orthop Clin North Am 1994;25:47-59. 3. Coughlin MJ, Schenck RC Jr, Shurnas PS, Bloome DM, Shurnas PJ. 109. Schon LC, Baxter DE. Neuropathies of the foot and ankle in athletes. Concurrent interdigital neuroma and MTP joint instability: long- Clin Sports Med 1990;9:489-509. term results of treatment. Foot Ankle Int 2002;23:1018-1025. 110. Schon LC, Baxter DE. Heel pain syndrome and entrapment neu- 4. Frey C, Kerr R. Magnetic resonance imaging and the evaluation of ropathies about the foot and ankle. In: Gould JS, editor. Operative tarsal tunnel syndrome. Foot Ankle 1993;14:159-164. foot surgery. Philadelphia: WB Saunders Co; 1994. p 192-208. 5. Gondring WH, Shields B, Wenger S. An outcomes analysis of surgi- 111. Schon LC, Easley ME. Chronic pain. In: Myerson MS, editor. Foot cal treatment of tarsal tunnel syndrome. Foot Ankle Int 2003;24:545- and ankle disorders. Philadelphia: WB Saunders Co; 2000. p 851- 550. 881. 6. Hort KR, DeOrio JK. Adjacent interdigital nerve irritation: single in- 112. Schon LC, Glennon TP, Baxter DE. Heel pain syndrome: electrodi- cision surgical treatment. Foot Ankle Int 2002;23:1026-1030. agnostic support for nerve entrapment. Foot Ankle 1993;14:129- 7. Kinoshita M, Okuda R, Morikawa J, Abe M. Tarsal tunnel syndrome 135. associated with an accessory muscle. Foot Ankle Int 2003;24:132- 113. Seiler JG. Double crush syndrome: experiemental model in the rat. 136. Forum 1983;34:597-597. 8. Labib SA, Gould JS, Rodriguez-del-Rio FA, Lyman S. Heel pain triad 114. Shapiro PP, Shapiro SL. Sonographic evaluation of interdigital neu- (HPT): the combination of plantar fasciitis, posterior tibial tendon romas. Foot Ankle Int 1995;16:604-606. dysfunction and tarsal tunnel syndrome. Foot Ankle Int 115. Skalley TC, Schon LC, Hinton RY, Myerson MS. Clinical results fol- 2002;23:212-220. lowing revision tibial nerve release. Foot Ankle Int 1994;15:360-367. 9. Lau JT, Daniels TR. Effects of tarsal tunnel release and stabilization 116. Stack RE, Bianco AJ, Jr., MacCarty CS. Compression of the procedures on tibial nerve tension in a surgically created pes planus common peroneal nerve by ganglion cysts: report of nine cases. J foot. Foot Ankle Int 1998;19:770-777. Bone Joint Surg Am 1965;47:773-778. 10. Oztuna V, Ozge A, Eskandari MM, Colak M, Golpinar A, Kuyurtar 117. Stein M, Shlamkovitch N, Finestone A, Milgrom C. Marcher’s digi- F. Nerve entrapment in painful heel syndrome. Foot Ankle Int talgia paresthetica among recruits. Foot Ankle 1989;9:312-313. 2002;23:208-211. AAEM Course Painful Foot and Ankle 51

11. Sammarco GJ, Chalk DE, Feibel JH. Tarsal tunnel syndrome and ad- 15. Skalley TC, Schon LC, Hinton RY, Myerson MS. Clinical results fol- ditional nerve lesions in the same limb. Foot Ankle 1993;14:71-77. lowing revision tibial nerve release. Foot Ankle Int 1994;15:360-367. 12. Sammarco GJ, Chang L. Outcome of surgical treatment of tarsal 16. Trepman E, Kadel NJ, Chisholm K, Razzano L. Effect of foot and tunnel syndrome. Foot Ankle Int 2003;24:125-131. ankle position on tarsal tunnel compartment pressure. Foot Ankle Int 13. Shapiro SL. Endoscopic decompression of the intermetatarsal nerve 1999;20:721-726. for Morton's neuroma. Foot Ankle Clin 2004;9:297-304. 17. Watson TS, Anderson RB, Davis WH, Kiebzak GM. Distal tarsal 14. Sharp RJ, Wade CM, Hennessy MS, Saxby TS. The role of MRI and tunnel release with partial plantar fasciotomy for chronic heel pain: ultrasound imaging in Morton's neuroma and the effect of size of an outcome analysis. Foot Ankle Int 2002;23:530-537. lesion on symptoms. J Bone Joint Surg Br 2003;85:999-1005. 52 AAEM Course AAEM Course 53 Painful Foot and Ankle

CME SELF-ASSESSMENT TEST

Select the ONE best answer for each question.

1. Anterior tarsal tunnel syndrome (TTS) is an isolated neu- 5. All of the following are true about the superficial peroneal ropathy involving the: nerve EXCEPT: A. Superficial peroneal nerve in the foot. A. It divides into the medial and intermediate dorsal cuta- B. Deep peroneal nerve at the ankle. neous branches in the distal leg. C. Deep peroneal nerve in the distal anterior compartment B. It passes deep to the inferior extensor retinaculum. of the leg. C. It pierces the deep crural fascia of the leg approximately D. Superficial peroneal nerve proximal to the ankle. 13 cm proximal to the tip of the lateral malleolus. E. Intermediate dorsal cutaneous branch of the superficial D. It innervates almost the entire dorsum of the foot. peroneal nerve. E. It innervates the dorsum of the first through fourth toes.

2. Anterior tarsal tunnel syndrome may present with: 6. Because the high amplitude zone for the extensor digitorum A. Aching in the ankle and distal leg. brevis (EDB) is so large, and because the belly of the muscle B. Numbness over the dorsum of the foot, sparing the first is so prominent, the E1 electrode for recording the CMAP dorsal web space. in this muscle can be placed anywhere over the bulk of the C. Weakness of dorsiflexion of the toes. muscle belly, as long as the distance from the stimulating D. Weakness of abduction of the toes. cathode is accurately measured. E. A and C. A. True. B. False. 3. The deep peroneal nerve often innervates the first dorsal interosseus manus. 7. In anterior TTS: A. True. A. The symptoms may be provoked by placing the patient’s B. False. foot in a “high-heeled shoe” position. B. Both the medial and lateral branches are always in- 4. Electrodiagnostic testing in anterior TTS may reveal: volved. A. Prolonged distal latencies in the deep peroneal nerve and C. An atrophic EDB suggests compromise of the medial superficial peroneal nerve across the ankle. branch. B. Spontaneous activity and decreased motor unit recruit- D. Numbness of the medial sole suggests compromise of ment in the extensor digitorum brevis. the medial branch. C. An abnormally small compound muscle action poten- E. A and C. tial (CMAP) in the superficial peroneal nerve to the foot. 8. The superficial peroneal nerve can be entrapped: D. An undetectable deep peroneal nerve sensory response A. Where it passes through the deep crural fascia of the across the ankle on both the affected foot and the unaf- distal leg. fected foot. B. Where it passes deep to the inferior extensor retinacu- E. Both B and D are correct. lum. C. Where it crosses the tendon of the extensor hallucis brevis in the dorsum of the foot. D. Where it crosses the medial malleolus. E. All of the above. 54 CME Self-Assessment Test AAEM Course

9. Patients with superficial peroneal nerve entrapment typically 15. Based on the information presented in this article, the most complain of numbness or paresthesias over the dorsum of the likely electrophysiologic abnormality in Baxter’s nerve en- foot. trapment would be: A. True. A. Reduced Baxter’s nerve CMAP amplitude. B. False. B. Prolonged distal onset latency of Baxter’s nerve. C. Decreased conduction velocity of Baxter’s nerve across 10. In superficial peroneal nerve entrapment, the following are the tarsal tunnel. true EXCEPT: D. Sustained fibrillation potentials or positive sharp waves A. The symptoms worsen at night. in the ADQP. B. Patients may actually report a localized mass in the distal E. Sustained fibrillation potentials or positive sharp waves anterolateral leg. in the flexor digitorum brevis. C. There may be a palpable bulge in the distal anterolateral leg. 16. The clinical differential diagnosis of TTS includes all of the D. There may be a palpable defect in the distal anterolateral following EXCEPT: leg. A. Plantar fasciitis. E. There is frequently impaired sensation over the dorsum B. Peripheral neuropathy. of the foot. C. L5 S1 radiculopathy. D. Proximal tibial neuropathy. 11.Baxter’s nerve usually DOES NOT innervate which of the E. Peripheral vascular disease. following: A. Abductor digiti quinti pedis (ADQP). 17. The most common cause of TTS is: B. Medial calcaneal tuberosity. A. Ganglion or schwannoma. C. Abductor hallucis. B. Tenosynovitis. D. Quadratus plantae. C. Trauma. E. Flexor digitorum brevis. D. Diabetic neuropathy. E. Rheumatoid arthritis. 12. The predominant clinical finding in Baxter’s nerve entrapment would be? 18. Medial and lateral plantar sensory nerve conduction studies A. Paresthesia in the heel. are easy to obtain without an averager. B. Pain in the medial/plantar aspect of the heel. A. True. C. Weakness of the fifth toe abductor. B. False. D. Altered gait pattern. E. Diminished Achilles’ reflex on the affected side. 19. Motor, sensory, and mixed nerve conduction studies (NCSs) along with needle electromyography can assist confirming 13. Which of the following is NOT considered to be a terminal the diagnosis of TTS in up to 90% of cases. branch of the tibial nerve? A. True. A. Baxter’s nerve. B. False. B. Medial plantar nerve. C. Medial calcaneal nerve. 20. For the diagnosis of TTS, sensory or mixed NCSs are much D. Lateral plantar nerve. more sensitive than the motor NCSs. E. Saphenous nerve. A. True. B. False. 14. All of the following are names for the nerve which innervates the ADQP muscle EXCEPT: 21. Testing of the lateral plantar motor nerve can best be per- A. Nerve to the abductor digiti quinti. formed by placing the active recording electrode over the B. Lateral calcaneal nerve. flexor digiti minimi brevis. C. Baxter’s nerve. A. True. D. 1st branch of the lateral plantar nerve. B. False. E. Inferior calcaneal nerve. AAEM Course CME Self-Assessment Test 55

22. TTS is the most common entrapment neuropathy of the 26. Which of the following statements about the posterior tibial tibial nerve. tendon is true? A. True. A. It everts the hind foot during toe-off. B. False. B. Problems with it lead to the development of pes cavus. C. It serves to balance the pull of the peroneal tendons. 23. The treatment of TTS includes all EXCEPT: D. Inflammation of it results in medial foot pain. A. Nonsteroidal anti-inflammatory drugs. E. It serves to balance the pull of the paroneal tendons. B. Corticosteroid injection. C. Epidural steroid injection. 27. Haglund’s syndrome involves all of the following, EXCEPT: D. Corrective orthosis. A. Insertional tendonitis. E. Surgical decompression of the tibial nerve at the ankle. B. Retrocalcaneal bursitis. C. Enlarged bursal prominence. 24. Which ligament is involved most commonly in a foot in- D. Isolated pump bump. version injury (ankle sprain)? E. Adentitial bursitis. A. Calcaneal fibular. B. Posterior talofibular. 28. Which one of the following is true about hallux rigidus? C. Anterior talofibular. A. It is arthritis of the first metatarsophalangeal joint D. Tibiocalcaneal. B. It usually does not cause pain E. None of the above. C. Is associated with diabetes mellitus D. Is caused by the contracture of the extensor hallucis 25. Which one of the following is the most common problem longus tendon in the hind foot? E. It develops as a result of pes planus (flat foot). A. Heel pad atrophy. B. Retrocalcaneal bursitis. C. Achilles tendonitis. D. Plantar fasciitis. E. Calcaneal stress fracture. 56 AAEM Course AAEM Course 57 Painful Foot and Ankle

EVALUATION

Select ANY of the answers that indicate your opinions. Your input is needed to critique our courses and to ensure that we use the best faculty instructors and provide the best course options in future years. Please use the computer form to answer the following questions. For the purpose of tabulating evaluations, please enter the last 4 digits of your telephone number in the ID NUMBER box beginning with the left column and fill in the appropriate ovals below each number. Make additional comments or list suggested topics or faculty for future courses on the comment form provided at the end.

29. How would you rate the quality of instruction received 33. How would you rate the quality of instruction received during Dr. Park’s presentation? during Dr. Saeed’s presentation? A. Best possible. A. Best possible. B. Good. B. Good. C. Average. C. Average. D. Fair. D. Fair. E. Worst possible. E. Worst possible.

30. Select any item(s), that, if changed, would have appreciably 34. Select any item(s), that, if changed, would have appreciably improved Dr. Park’s presentation: improved Dr. Saeed’s presentation: A. Quality of slides. A. Quality of slides. B. Quality of handout. B. Quality of handout. C. Amount of clinically relevant information in the presen- C. Amount of clinically relevant information in the presentation. tation. D. Amount of scientific content in the presentation. D. Amount of scientific content in the presentation. E. Other: please explain on the comment form at the back E. Other: please explain on the comment form at the back of this handout. of this handout.

31. How would you rate the quality of instruction received 35. How would you rate the quality of instruction received during Dr. Del Toro’s presentation? during Dr. Patel’s presentation? A. Best possible. A. Best possible. B. Good. B. Good. C. Average. C. Average. D. Fair. D. Fair. E. Worst possible. E. Worst possible.

32. Select any item(s), that, if changed, would have appreciably 36. Select any item(s), that, if changed, would have appreciably improved Dr. Del Toro’s presentation: improved Dr. Patel’s presentation: A. Quality of slides. A. Quality of slides. B. Quality of handout. B. Quality of handout. C. Amount of clinically relevant information in the presen- C. Amount of clinically relevant information in the presentation. tation. D. Amount of scientific content in the presentation. D. Amount of scientific content in the presentation. E. Other: please explain on the comment form at the back E. Other: please explain on the comment form at the back of this handout. of this handout. 58 Evaluation AAEM Course

37. How would you rate the quality of instruction received 40. Select ALL items where improvement was needed. during Dr. Easley’s presentation? A. The accuracy of advance descriptions of this course. A. Best possible. B. The specific topics selected for presentation. B. Good. C. The number of speakers in this course. C. Average. D. The amount of time allotted for discussion in this D. Fair. course. E. Worst possible. E. Other: please add other areas and outline specific recommendations for areas needing improvement on the 38. Select any item(s), that, if changed, would have appreciably comment form at the back of this handout. improved Dr. Easley’s presentation: A. Quality of slides. 41. Should this topic be presented in the future by a different B. Quality of handout. method of presentation. C. Amount of clinically relevant information in the presen- A. No, the topic of presentation should remain as a course. tation. B. Yes, the topic should be presented as a dinner seminar. D. Amount of scientific content in the presentation. C. Yes, the topic should be incorporated into the plenary E. Other: please explain on the comment form at the back session. of this handout. D. Yes, the topic should be discussed during a breakfast session. 39. As a result of your attendance at this course, did you learn E. Yes, the topic should be organized as a special interest anything that will improve the care of your patients? group. A. Yes, substantially. B. Yes, somewhat. C. Not sure. D. Probably not. E. This course was not applicable to my patients. AAEM Course 59 FUTURE MEETING RECOMMENDATIONS

Select ANY of the answers that indicate your opinions. The following questions are included with all dinner seminar, course, and plenary session evaluations. It is only necessary to answer these questions once during the course of the entire meeting.

42. Please indicate below your specialty: 48. How would you rate this meeting? A. Neurologist. A. Poor. B. Physiatrist. B. Fair. C. PhD. C. Good. D. Other. D. Very good. E. Excellent. 43. How often do you attend AAEM meetings? A. Annually. 49. Did this meeting meet your expectations? B. Every 2-3 years. A. Not at all. C. Every 4 or more years. B. Somewhat. D. This is the first AAEM meeting I have attended. C. As expected. D. Exceeded expectations. 44. With regard to this years meeting, which of the smaller E. Best ever. group sessions did you attend? (mark all that apply) A. Experts’ roundtables. 50. Was the printed program clear and easy to follow? B. Workshops. A. Yes. C. Dinner seminars. B. No. D. None of the above. 51. With regard to the meeting hotels: 45. If you answered none of the above to the previous question, A. I stayed at one of the meeting hotels. please answer the following. The reason I did not attend the B. I did not stay at one of the meeting hotels. small group sessions was due to: A. The timing of the event. 52. If you answered B to the question above, please explain why B. The cost of the event. you did not stay at one of the meeting hotels (please make C. My lack of interest in the topics offered. your comments under Comments, page 61). D. The session was full. 53. How did you first learn about the meeting? (choose the 46. Did this meeting provide information that will enhance care method where you first learned about the meeting) of your patients? A. Preliminary brochure mailing. A. Extremely. B. Registration brochure mailing. B. Somewhat. C. The internet. C. Very little. D. Email message. D. Not at all. E. From a friend.

47. With regard to the social event: 54. Did you perceive any commercial bias in any of the educa- A. I am signed up to attend the social event. tional sessions offered by the AAEM at this meeting? B. I did not sign up because of the cost of the event. A. Yes. C. I did not sign up because of the day the event was B. No. offered. D. I did not sign up because I am not interested in attend- 55. Did you attend any of the industry forums provided this ing this type of function. year? A. Yes. B. No. 60 Future Meeting Recommendations AAEM Course

56. If you answered yes to question 55 and you attended the 58. How do you prefer to learn new information? Pfizer Industry Forum, how would you rate the quality of the A. Lecture only. session? B. Lecture in conjunction with questions and answers. A. Best possible. C. Small group hands-on. B. Good. D. Small group discussion. C. Average. D. Fair. 59. I plan to attend the 2005 AAEM meeting in Monterey, E. Worst possible. California, September 21-24. On Page 61 under comments, please provide any other A. Yes, definitely. comments you have about your attendance at the Pfizer B. No, definitely. Industry Forum. C. Will wait to see the program content. D. Will wait to see if budget allows my attendance. 57. If you answered yes to question 55 and you attended the Allergan Industry Forum, how would you rate the quality of 60. I would be more likely to attend the 2005 AAEM meeting if the session? (please make your comments under Comments, page 61): A. Best possible. B. Good. C. Average. D. Fair. E. Worst possible. On Page 61 under comments, please provide any other comments you have about your attendance at the Allergan Industry Forum. COMMENTS

Given time and budget constraints, is there something we could do in terms of altering the format of the meeting that would significantly increase the likelihood of your attendance at future AAEM meetings? Explain:

Write out any additional comments about specific courses or the plenary session (please indicate which), and list suggestions for topics and speakers for future meetings. Leave at the AAEM Registration and Information Center or mail to the AAEM Executive Office at 421 First Avenue SW, Suite 300 East, Rochester, MN 55902. AAEM 421 First Avenue SW, Suite 300 East Rochester, MN 55902 (507) 288-0100 / Fax: (507) 288-1225 [email protected] www.aaem.net